Table of Content

05 February 2026, Volume 46 Issue 2

Previous Issue   

Original Articles

SilicosisOmics: an integrated multi-omics platform for silicosis

WANG Jixin, HUANG Xinlei, QI Xianmei, ZHANG Tiantian, PANG Junling, LONG Erping, WANG Jing

2026, 46(2):  155-163.  doi:10.16352/j.issn.1001-6325.2026.02.0155

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Objective To address the challenges of fragmented multi-omics data and insufficient integrated analysis in silicosis research, we aim to construct a comprehensive data platform that supports systematic analysis of multi-level molecular alterations in fibrotic lung tissues and facilitates rapid identification of therapeutic targets. Methods We systematically integrated transcriptomic, single-cell transcriptomic, quantitative proteomic, post-translational modification-specific proteomic, and metabolomic data from human and mouse silicotic and control lung tissues. By leveraging bioinformatics tools including DESeq2, Seurat, and CellChat, we developed a web-based visualization platform enabling data visualization and interactive analysis. Results We successfully constructed SilicosisOmics (https://respir.pumc.edu.cn/SilicosisOmics/), a comprehensive multi-omics data platform for silicosis research. The platform integrated five types of omics data derived from both silicotic and non-diseased lung tissues across human and mouse species. SilicosisOmics provided not only online search functionality for static visualization of gene expression and single-cell clustering but also interactive analytical tools supporting user-customized analyses including differential gene expression, pathway enrichment, and cell-cell interaction studies. Conclusions The SilicosisOmics platform offers systematic multi-omics data resources and user-friendly analytical tools for silicosis and pulmonary fibrosis research, thereby facilitating the advancement of mechanistic studies, target discovery, and subsequent translational research.

Qingshi anti-itch ointment alleviaties imiquimod-induced psoriatic skin lesions in mice

CUI Yudi, ZHANG Fengchuan, LI Yuanwen, YANG Bilian

2026, 46(2):  164-169.  doi:10.16352/j.issn.1001-6325.2026.02.0164

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Objective To investigate the therapeutic effect and underlying mechanism of Qingshi anti-itch ointment (QAO) on imiquimod-induced psoriatic skin lesions in mice. Methods Mice were randomly divided into five groups: the control, model, low-dose QAO, high-dose QAO, and positive drug groups. Skin lesions were evaluated using the PASI scoring system, and histopathological changes were observed via HE staining. The protein levels of p65, IκBα, NLRP3, ASC, and caspase-1 in skin tissue were analyzed by Western blot. RT-qPCR was used to measure the mRNA expression of p65 and IκBα. Serum levels of IL-1β, IL-18, TNF-α, and IFN-γ were quantified by ELISA. Results Compared with the control group, the model group exhibited significant erythema, scaling, and skin thickening, accompanied by increased PASI scores, elevated pro-inflammatory cytokines (IL-1β/IL-18), upregulated NLRP3/ASC/caspase-1 proteins, and activated NF-κB signaling (increased p65 and decreased IκBα). Treatment with QAO and positive drug effectively reduced PASI scores, improved skin symptoms, suppressed NLRP3 inflammasome activation, and restored the NF-κB/IκBα balance (all P＜0.05). Conclusions QAO alleviates psoriatic skin lesions in mice by inhibiting the NF-κB/NLRP3 signaling axis, thereby reducing pro-inflammatory cytokine production and inflammatory responses.

miR-218-5p alleviates high glucose-induced injury in mouse podocyte MPC5

YU Yuan, HU Yiqiong, XIANG Qingwei

2026, 46(2):  170-176.  doi:10.16352/j.issn.1001-6325.2026.02.0170

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Objective To investigate the effect of miR-218-5p on high glucose (HG)-induced injury in a mouse podocyte cell line MPC5 and its potential mechanism involving targeting tissue inhibitor of metalloproteinase 2 (TIMP2). Methods MPC5 cells were divided into the following groups: control group, HG group, NC-mimics group, miR-218-5p-mimics group, miR-218-5p-mimics+pcDNA-NC group, and miR-218-5p-mimics+pcDNA-TIMP2 group. All groups except the control group were treated with 30 mmol/L glucose for 24 hours to induce injury.The expression levels of miR-218-5p and TIMP2 mRNA were detected by RT-qPCR. Cell proliferation and apoptosis were assessed using the CCK-8 assay and flow cytometry, respectively. The activities of reactive oxygen species (ROS) and superoxide dismutase (SOD), as well as the content of malondialdehyde (MDA), were measured using ELISA kits. Protein expression levels were detected by Western blot. The targeting relationship between miR-218-5p and TIMP2 was verified by a dual-luciferase reporter assay. Results Compared with the control group, the HG group showed decreased A₄₅₀ value, miR-218-5p expression, and SOD activity, but increased apoptosis rate, TIMP2 mRNA and protein expression, ROS activity, MDA content, and cleaved caspase-3 expression (P＜0.05). Compared with the HG and NC-mimics groups, the miR-218-5p-mimics group exhibited an increased A₄₅₀ value, elevated miR-218-5p expression, and higher SOD activity, whereas the apoptosis rate, TIMP2 mRNA and protein expression, ROS activity, MDA content, and cleaved caspase-3 expression were decreased (P＜0.05). Furthermore, compared with the miR-218-5p-mimics group and the miR-218-5p-mimics+pcDNA-NC group, the miR-218-5p-mimics+pcDNA-TIMP2 group displayed a reduced A₄₅₀ value and SOD activity, alongside an increased apoptosis rate, elevated TIMP2 mRNA and protein expression, higher ROS activity, increased MDA content, and enhanced cleaved caspase-3 expression (P＜0.05).The dual-luciferase reporter assay confirmed that miR-218-5p could directly target and negatively regulate TIMP2. Conclusions Overexpression of miR-218-5p protects against HG-induced podocyte injury, and this protective effect may be mediated through the negative regulation of TIMP2.

Effect of IKKε kinase on hypoxic injury of rat cardiomyocyte H9c2

GUO Weichong, LI Chen, HU Mingzhen, FAN Lin, CAI Xiaohang, TAN Xin, MA Jinxia

2026, 46(2):  177-185.  doi:10.16352/j.issn.1001-6325.2026.02.0177

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Objective To investigate the effect of IKKε kinase on hypoxic injury in rat cardiomyocyte cell line H9c2. Methods H9c2 cells, H9c2 cells with IKKε knockdown or overexpression, were cultured in vitro. A hypoxic injury model was established using H9c2 cells. The cells were divided into the following groups: normal control, acute hypoxia, IKKε overexpression, IKKε knockdown, acute hypoxia + IKKε overexpression, and acute hypoxia + IKKε knockdown. The CCK-8 assay was used to detect cell viability. A commercial kit was used to detect the activity of lactate dehydrogenase (lactate dehydrogenase, LDH). Lyso-Tracker staining was employed to detect the level of lysosomal acidification. Immunofluorescence was used to detect the expressions of Beclin-1, LC3-Ⅱ/Ⅰ, and IL-1β. ELISA was applied to detect the concentration of IL-1β. Western blot was carried out to detect the expressions of IKKε, autophagy-related proteins (Beclin-1, LC3, p62), and apoptosis-related proteins (Bcl-2, Caspase-3, Bax). Results Compared with the normal control group, the viability of H9c2 cardiomyocytes in the acute hypoxia control group was weakened, the LDH activity was significantly increased, the level of lysosomal acidification was significantly decreased, autophagy was enhanced, and apoptosis was increased. Compared with the acute hypoxia group, the acute hypoxia + IKKε knockdown group exhibited enhanced cell viability, significantly decreased LDH activity, enhanced autophagy, reduced apoptosis, and an attenuated inflammatory response. The acute hypoxia + IKKε overexpression group showed results opposite to those of the acute hypoxia + IKKε knockdown group. Conclusions Knocking down IKKε can alleviate hypoxic-induced injury in H9c2 cardiomyocytes, and the mechanism may be related to enhanced autophagy, reduced apoptosis, and an attenuated inflammatory response.

LINC01123 promotes cell proliferation of colorectal cancer in vivo by regulating miR-625-5p/LASP1 signaling axis

ZHANG Tingting, XU Yiping, SHANG Tao

2026, 46(2):  186-192.  doi:10.16352/j.issn.1001-6325.2026.02.0186

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Objective To investigate whether LINC01123 promotes colorectal cancer (CRC) cell proliferation through regulating the miR-625-5p/LASP1 signaling axis. Methods SSW480 cells were cultured, and and then divided into sh-NC, sh-LINC01123 and sh-LINC01123+miR-625-5p inhibitor groups. An in vivo xenograft tumor model was established in nude mice, and the tumor volume and tumor weight were detected. HE staining was used to detect the pathological changes of tumor tissues, TUNEL staining was used to detect cell apoptosis, and immunohistochemical(IHC) assay was used to detect the expressions of Ki-67 and LASP1 proteins in nude mouse tumor tissues. The mRNA expressionsof LINC01123, miR-625-5p and LASP1 were detected by RT-qPCR, and the protein expressions of LINC01123 and LASP1 were detected by Western blot. Results Compared with the sh-NC group, the sh-LINC01123 group showed significantly decreased tumor volume, expression of Ki-67 and LASP1 protein, mRNA levels of LINC01123 and LASP1 in sh-LINC01123 group were significantly decreased (P＜0.05). Tumor tissue structure was severely disrupted, with widespread cell pyknosis and necrosis. Meanwhile, the TUNEL-positive cell rate and miR-625-5p mRNA expression were significantly increased(P＜0.01). In contrast, compared with sh-LINC01123 group, tumor volume, expression of Ki-67, LASP1 protein and mRNA expression of LINC01123 and LASP1 in sh-LINC01123+miR-625-5p inhibitor group were significantly increased, and tumor tissue growth was significantly inhibited (P＜0.05), the TUNEL-positive cell rate and miR-625-5p mRNA expression were significantly decreased(P＜0.01). Conclusions LINC01123 can promote the proliferation of colorectal cancer in vivo by regulating miR-625-5p/LASP1 signaling axis.

Liraglutide decreases cardiac function damage and atrial fibrillation susceptibility in rats with myocardial infarction

LI Jingwei, ZHANG Runfeng

2026, 46(2):  193-199.  doi:10.16352/j.issn.1001-6325.2026.02.0193

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Objective To investigate the effects of liraglutide on myocardial inflammation and cardiac function in rats with acute myocardial infarction (AMI), and to further explore its effects on susceptibility to atrial fibrillation and the underlying mechanisms. Methods The rats were divided into the sham operation group (sham group), the AMI group(using the method of coronary arteryligation), and the liraglutide group (AMI+LIR group). Rats in the AMI + LIR group were intraperitoneally injected with liraglutide at a dose of 250 μg/ (kg·d).The sham group and the AMI group were injected with an equal amount of normal saline. Four weeks later, echocardiography was used to evaluate the cardiac structure and function of the rats; electrocardiogram was collected and electrophysiological detection was performed to evaluate the susceptibility to atrial fibrillation; HE staining and Masson staining were used to detect the morphology of myocardial cells and the degree of myocardial fibrosis; the enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-18 (IL-18); Western blot was used to detect the protein expressions of NLRP3, Caspase-1, and GSDMD in the myocardial tissues. Results Compared with the sham group, the degree of myocardial fibrosis and the infiltration of inflammatory cells in the myocardial tissue of the rats in the AMI group increased significantly; the left atrial diameter (LAD), the left ventricular posterior wall thickness after diastole (LVPWd), and the left ventricular end-diastolic diameter (LVEDd) were significantly increased, while the left ventricular fractional shortening (FS) and the left ventricular ejection fraction (LVEF) were significantly decreased (P＜0.05); The P-wave duration (PWD), PR interval (PRI), and maximum absolute fibrillation duration (MAFD) increased, while the atrial effective refractory period (AERP)was decreased; the levels of inflammatory factors IL-6, IL-18, IL-1β and the protein expressions of NLRP3, Caspase-1, and GSDMD were significantly increased (P＜0.05). Compared with the AMI group, the myocardial fibrosis and inflammatory infiltration in the AMI+LIR group were improved; the LAD, LVPWd, and LVEDd were significantly decreased, while the FS and LVEF were significantly increased; the levels of inflammatory factors IL-6, IL-18, IL-1β and the protein expressions of NLRP3, Caspase-1, and GSDMD were significantly decreased(P＜0.05). Conclusions Liraglutide can reduce myocardial fibrosis and inflammation, improve cardiac function, and decrease the susceptibility to atrial fibrillation in rats with AMI.

Renal sympathetic denervation alleviates cardiac and renal damage in rats with chronic kidney disease

DONG Jian, XU Jie, ZHAO Liang, LUO Xiaomei

2026, 46(2):  200-207.  doi:10.16352/j.issn.1001-6325.2026.02.0200

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Objective To investigate the cardiorenal protective effects of renal sympathetic denervation(RSD) in rats with chronic kidney disease (CKD). Methods Rats were divided into five groups (n=6 per group): sham-operated group,5/6 nephrectomy-induced chronic kidney injury (CKI) model group, RSD group, metoprolol group, and perindopril group. Systolic blood pressure (SBP) and heart rate were measured noninvasively using the tail-cuff method at weeks 4 and 8. Cardiac ultrasonography was performed to assess left ventricular end-diastolic posterior wall thickness (PWTd), interventricular septal thickness at end-diastole (IVSTd),ejection fraction (LVEF), and left ventricular mass (LV mass). Blood and urine samples were collected for biochemical analysis. At week 8, heart and kidney tissues were collected for histopathological examination. Masson's trichrome staining was used to evaluate cardiac and renal fibrosis. Serum levels of IL-1β, IL-6, TNF-α, and TGF-β1 were measured by ELISA. Protein expression of Smad2/3, p-Smad2/3, α-SMA, Collagen1, and TGF-β1 in cardiac tissue was analyzed by Western blot. Results Compared with the sham group, the model group exhibited significantly elevated SBP, increased IVSTd, LVPWd, and LV mass, higher levels of urinary protein (UP), creatinine (Cr), blood urea nitrogen (BUN), uric acid (UA), and brain natriuretic peptide (BNP) and reduced LVEF as well as kidney volume (K Vol)(all P＜0.05). In contrast, all intervention groups (RSD, metoprolol, perindopril) exhibited significant reductions in SBP, IVSTd, LVPWd, LV mass, and lower levels of UP, Cr, BUN, UA, and BNP, as well as improved LVEF compared to the model group (P＜0.05). The model group had elevated serum level of all four inflammatory cytokines. In contrast, the RSD, metoprolol, and perindopril groups exhibited significant reductions in IL-6 and TGF-β1 compared to the model group (P＜0.05). Histopathological analysis revealed disorganized myocardial fibers with interstitial fibrosis in the model group, as well asglomerular atrophy, tubular degeneration/dilation, and marked interstitial fibrosis with inflammatory infiltration in renal tissue. All intervention groups (RSD, metoprolol, perindopril) showed attenuated fibrotic changes (P＜0.05). Tyrosine hydroxylase (TH) immunostaining showed greater sympathetic activation in the model group, which was ameliorated by all interventions (P＜0.05). Western blot analysis confirmed up-regulated cardiac expression of TGF-β1, p-Smad2/3, α-SMA, and Collagen Ⅰ(P＜0.05). These fibrotic markers were significantly downregulated in all treatment groups relative to the model group (P＜0.05), with perindopril showing the most pronounced effects. Conclusions Renal sympathetic denervation alleviates cardiorenal injury in CKD rats by mitigating fibrosis and suppressing IL-6/TGF-β1-mediated inflammation.

Regulatory effects of Jinmaitong on high glucose-induced glycolytic reprogramming in RSC96 cells and polarization of RAW264.7 cells

CHE Yanfei, QIN Dongshan, YU Ziman, WANG Haoyu, YANG Dan, LIANG Xiaochun

2026, 46(2):  208-214.  doi:10.16352/j.issn.1001-6325.2026.02.0208

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Objective To investigate the regulatory effects of Jinmaitong on glycolysis and histone lactylation in high glucose-induced rat Schwann cell line RSC96, and its impact on macrophage polarization. Methods A high-glucose metabolic stress model was established using RSC96 cells, followed by treatment with different concentrations of Jinmaitong. Cell proliferation, lactate levels, and the expression of glycolytic enzymes (PKM2, LDHA) and histone lactylation marker H3K18la were assessed to evaluate metabolic and epigenetic changes. In addition, conditioned media from high-glucose-treated RSC96 cells were applied to RAW264.7 macrophages to examine changes in polarization-related phenotypic markers. Results High-glucose stimulation enhanced glycolytic activity and lactate accumulation in RSC96 cells, accompanied by upregulation of H3K18la modification, indicating a state of metabolic stress. Jinmaitong treatment led to a dose-dependent reduction in glycolytic enzyme expression and lactate levels, and significantly suppressed H3K18la expression. Conditioned media from high-glucose-treated Schwann cells promoted M1 polarization of RAW264.7 cells, whereas Jinmaitong intervention reversed this trend, promoting M2 polarization and alleviating the pro-inflammatory microenvironment. Conclusions High-glucose conditions induce glycolytic reprogramming and histone lactylation in Schwann cells, which may contribute to macrophage polarization and neural injury.

Impact of different intervention methods on smoking cessation

ZHANG Yi, LONG Meiling, LI Xingchen, TONG Jin

2026, 46(2):  215-219.  doi:10.16352/j.issn.1001-6325.2026.02.0215

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Objective To evaluate different intervention methods on the efficacy of smoking cessation in order to support individualized and precise smoking cessation. Methods Data of 368 patients who visited the smoking cessation clinic at the Second Affiliated Hospital of Chongqing Medical University from October 2021 to October 2023 were collected and divided into outpatient group, WeChat group and outpatient+WeChat group according to their preferences. Statistical analysis of social demographic characteristics, smoking and smoking cessation status in each group was performed. Results At the third and sixth months, the WeChat group had the lowest smoking reduction rate, sustained smoking cessation rate, and 7-day point-prevalence abstinence rate in the third month, as well as the highest dropout rate (all P＜0.05); In the sixth month, the outpatient+WeChat group had the highest continuous smoking cessation rate and the WeChat group had the lowest (both P＜0.05). In the sixth month, the number of cigarette reduction in each group increased compared to before, with the outpatient+WeChat group having the highest number of cigarette reductions (P＜0.05). The degree of tobacco dependence decreased compared to before and the FTND and HSI scores of the WeChat group were higher than the other two groups (both P＜0.05). Age, degree of tobacco dependence, and completion of long-term follow-up were risk factors for successful smoking cessation (all P＜0.05). Conclusions Different methods can help quit smoking and the intervention effect of outpatient+WeChat group is the most effective one and the WeChat group is the weakest one.

Association between macrophage count and neutrophil extracellular trap content in thrombi of acute ischemic stroke patients

ZANG Mingming, HAN Ruodong, YAN Xiuxia

2026, 46(2):  220-226.  doi:10.16352/j.issn.1001-6325.2026.02.0220

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Objective To explore the correlation between the number of macrophages and neutrophil extra cellular traps (NETs) in thrombi of patients with acute ischemic stroke (AIS), and to compare the NET-degrading and clearing abilities of macrophages in different polarization states. Methods Immunohistochemical staining was performed to detect CD16⁺ macrophages, CD163⁺ macrophages and citrullinated histone 3(CitH3) in AIS thrombi. Thrombi were co-cultured with macrophages, and the CitH3 concentration in the supernatant was measured to evaluate the NET-degrading and clearing capacities of different macrophage subtypes. Results All 30 thrombi showed positive expression of CD16 macrophages, CD163 macrophages and CitH3. The numbers of both CD16⁺ and CD163⁺ macrophages were positively correlated with the percentage of CitH3-positive area (CD16: r=0.538, P＜0.05; CD163: r=0.641, P＜0.001). After co-culture, the CitH3 concentration was significantly lower in both the M1- and M2- macrophage groups than in the blank control group (M1: t=-3.981, P＜0.001; M2: t=-2.057, P＜0.05). The concentration of CitH3 was lower in the M1 group than in the M2 group (t=-2.125, P＜0.05). Conclusions Both M1 and M2 macrophage infiltration are correlated with NET content in AIS thrombi, and their abilities to clear and degrade NETs are different.

Propofol pretreatment alleviates focal cerebral ischemia-reperfusion injury in rats

XIA Honglian, ZHANG Yanli, ZHONG Weiwei, LIU Yongliang, CHEN Meng, CUI Honglei

2026, 46(2):  227-232.  doi:10.16352/j.issn.1001-6325.2026.02.0227

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Objective To investigate whether propofol pretreatment can reduce neurological damage induced by focal cerebral ischemia-reperfusion (I/R) injury in rats. Methods A rat middle cerebral artery occlusion (MCAO) model was established to induce focal cerebral ischemia. Rats were randomly assigned to four groups (n=12 per group): sham, MCAO, propofol, and propofol + ErbB4 antagonist (propofol + PD158780). Neurological function was evaluated using the neurological severity score (NSS), infarct volume was measured by TTC staining, neuronal pathological morphology was assessed by HE staining microscopy and Bcl-2 protein content was quantified by Western blot. Results Compared to sham controls, MCAO group exhibited significantly higher NSS scores (P＜0.05), larger cerebral infarction volume (P＜0.05), and more severe neuronal damage in the cerebral cortex (P＜0.05), while the expression of Bcl-2 protein in brain tissue remained unchanged(P＞0.05).Compared to the MCAO group, the propofol group exhibited significantly lower NSS scores (P＜0.05), reduced infarct volume(P＜0.05), alleviated neuronal damage in the cerebral cortex (P＜0.05), and significantly increased Bcl-2 expression (P＜0.05). Compared to the propofol group, the propofol+PD158780 group demonstrated significantly increased NSS scores (P＜0.05), larger infarct volume (P＜0.05), aggravated neuronal damage (P＜0.05), and decreased Bcl-2 expression (P＜0.05). Conclusions Propofol pretreatment may attenuate cerebral I/R-induced neurological damage via the Nrg-1β/ErbB4 signaling pathway.

Palladin promotes the stem features of gliomas cell line U251 through activating the mTOR pathway

ZHAO Kaitao, MIAO Rui, WANG Wei

2026, 46(2):  233-240.  doi:10.16352/j.issn.1001-6325.2026.02.0233

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Objective To investigate the promoting effect of Palladin on the stemness characteristics of glioma and explore potential novel therapeutic targets for glioma treatment. Methods Tumor stem cells were enriched from glioma U251 cells by sphere culture, and the expression level of Palladin was compared between these stem cells and parental cells using Western blot. Stable U251 cell lines with Palladin overexpression and knockdown were established. Sphere formation, Transwell invasion and drug resistance assays were performed to evaluate the self-renewal capacity, metastatic potential and drug resistance of these cells. Additionally, colony formation and CCK-8 assays were used to analyze proliferative capacity across all cell groups. The molecular mechanism of Palldin was investigated using Western blot and rescue experiments. Results Sphere-forming cells exhibited statistically significant upregulation of Palladin expression compared to parental cells. Sphere formation assays, Transwell invasion assays, and drug resistance assays demonstrated that Palladin overexpressing U251 cells exhibited significantly enhanced self-renewal capacity, invasive potential, and drug resistance compared to control cells, whereas Palladin-knockdown U251 cells showed markedly reduced self-renewal, invasion, and drug resistance capabilities. Colony formation and CCK-8 assays demonstrated that over-expression of Palladin enhanced proliferation of U251 cells, while knockdown of Palladin significantly reduced their proliferation. Western blot and rescue experiments further revealed that Palladin exerts its functional effected through activation of the mTOR signaling pathway. Conclusions Palladin promotes glioma stemness characteristics through activation of the mTOR pathway, highlighting its potential value as a therapeutic target.

Saikosaponin D inhibits TGF-β1-induced expression of fibrosis-related proteins in HFL1 human fetal lung fibroblasts

MIN Rui, LI Da, XU Yuxiang

2026, 46(2):  241-249.  doi:10.16352/j.issn.1001-6325.2026.02.0241

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Objective To investigate the therapeutic effects of saikosaponin D (SSD) on idiopathic pulmonary fibrosis(IPF). Methods Human fetal lung fibroblasts HFL1 cells were divided into control, model (TGF-β1, 5 ng/mL), SSD intervention (2.5/5/10 μmol/L), and positive control (rapamycin, 20 nmol/L) groups. Cell proliferation was assessed by CCK-8 assay; the expression of fibrosis- and pyroptosis-related protein were determined by Western blot; the expression of fibrosis-related genes was measured by RT-qPCR; cell damage was evaluated by LDH release assay; apoptosis was examined by flow cytometry; pyroptosis-related protein level was detected by immunofluorescence method and pyroptosis was observed by microscopy. Results Compared with the control group, TGF-β1 significantly promoted HFL1 cell proliferation (P＜0.05); compared with the model group, SSD inhibited cell proliferation in a concentration-dependent manner (P＜0.05). Compared with the control group, the expression of key proteins in the mTORC1/4E-BP1 pathway and pyroptosis-related proteins was significantly increased in the model group (P＜0.05); compared with the model group, their expression was significantly decreased in the SSD-treated groups (P＜0.05). Compared with the control group, the mRNA expression of fibronectin, collagen I, IL-1β, and IL-18 was significantly increased in the model group (P＜0.05); compared with the model group, their expression was significantly decreased after SSD treatment (P＜0.05). Compared with the control group, LDH release was significantly increased in the model group (P＜0.05); compared with the model group, it was significantly decreased in the SSD-treated groups (P＜0.05). Immunofluorescence showed that the expression of Ki67 and vimentin was significantly increased in the model group compared with the control group (P＜0.05), and was significantly decreased after SSD treatment compared with the model group (P＜0.05). Conclusions SSD alleviates TGF-β1-induced pulmonary fibrosis by inhibiting pyroptosis, reducing fibrotic protein expression and suppressing inflammatory cytokine release.

Farnesoid X receptor suppresses pancreatic cancer cell proliferation through negative regulation of matrix metalloproteinase 7

LI Zhitao, BU Xuefeng, ZHANG Yongjun, MENG Nana, XIA Leizhou

2026, 46(2):  250-255.  doi:10.16352/j.issn.1001-6325.2026.02.0250

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Objective To investigate the correlation between the expression of farnesoid X receptor (FXR) and matrix metalloproteinase 7 (MMP7) in pancreatic cancer cells, and to elucidate the role of FXR in regulating pancreatic cancer cell proliferation. Methods The effects of FXR on proliferation and MMP7 expression in pancreatic cancer cells (BxPC-3, PANC-1) were evaluated by in vitro experiments (CCK-8 assay, RT-PCR and Western blot). Bioinformatics analysis using GEPIA2 was performed to assess FXR/MMP7 expression and clinical prognosis in pancreatic cancer tissues, with immunohistochemistry (IHC) validating their correlation. Results FXR activation by GW4064 significantly inhibited pancreatic cancer cell proliferation (P＜0.05) and down-regulated MMP7 mRNA and protein levels (P＜0.01); while FXR inhibition by NDB significantly increased pancreatic cancer cell proliferation (P＜0.01) and upregulated the expression of MMP7 mRNA and protein(P＜0.001,P＜0.01). Bioinformatics analysis indicated that MMP7 was highly expressed in pancreatic adenocarcinoma tissues (P＜0.05), and its high expression was significantly associated with poor patient prognosis (P＜0.05); while no statistically significant association was found between FXR and prognosis. IHC (n=16) suggested an inverse correlation between FXR and MMP7 expression (R²=0.536 9). Conclusions FXR suppresses pancreatic cancer cell proliferation by negatively regulating MMP7, suggesting the BA(bile acid)-FXR-MMP7 axis as a potential therapeutic target.

Clinical Sciences

Correlation between serum PLR, SII, and Cys C levels and the vascular recanalization after mechanical thrombectomy in patients with acute cerebral infarction due to large vessel occlusion

PEI Shuang, SUN Jun, WANG Ning, ZHANG Qi, ZHANG Zaihang, BAI Fanghui, WEN Changming

2026, 46(2):  256-260.  doi:10.16352/j.issn.1001-6325.2026.02.0256

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Objective To investigate the correlation and significance of the ratio of serum platelet to lymphocyte count ratio(PLR), systemic inflammatory response index (SII), cystatin C (Cys C) in blood with the degree of vascular recanalization in patients with acute cerebral infarction due to large vessel occlusion after mechanical thrombectomy. Methods Two hundred patients with acute cerebral infarction due to large vessel occlusion were admitted to Nanyang Central Hospital from April 2021 to May 2024 were selected. They were categorized into a complete group and an incomplete group based on whether the blood vessel reopened completely after thrombectomy. The baseline data, preoperative PLR, SII, and Cys C levels were compared between the two groups. The correlation betweenPLR, SII, and Cys C and the degree of blood vessel reopening after thrombectomy, as well as their predictive value for complete blood vessel reopening, were analyzed. Results The proportion of patients with incomplete group high thrombus burden, puncture to recanalization time, PLR, SII, and Cys C were higher in the complete group(P＜0.05); Spearman correlation analysis showed that PLR, SII, and Cys C were negatively correlated with the degree of vascular recanalization (P＜0.001); partial correlation analysis, after adjusting for confounding factors, showed that PLR, SII, and Cys C remained significantly correlated with the degree of vascular recanalization after thrombectomy (P＜0.001); ROC analysis showed that among single factors, Cys C had the highest AUC for predicting complete vascular recanalization, and the AUC of PLR+SII+Cys C was greater than that of Cys C (P＜0.05). Conclusions PLR, SII, and Cys C are associated with the degree of vascular recanalization after mechanical thrombectomy in patients with acute cerebral infarction due to large vessel occlusion, which are potential markers for predicting the degree of vascular recanalization. The combined detection of the three can further improve predictive performance, providing important reference information for early clinical prediction of reflow conditions and treatment.

Association of MICA and CXCR1 with prognosis in children with severe pneumonia

WANG Tianjiao, SONG Yiqin, WANG Jing

2026, 46(2):  261-266.  doi:10.16352/j.issn.1001-6325.2026.02.0261

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Objective To investigate the relationship between serum levels of major histocompatibility complex class Ⅰ chain-related molecule A (MICA) and C-X-C motif chemokine receptor 1 (CXCR1) and the immune function and clinical prognosis of children with severe pneumonia. Methods A total of 202 children with severe pneumonia who visited Baoding Hospital, Beijing Children's Hospital Capital Medical University from January 2021 to January 2024 were enrolled as research group, which were divided into good prognosis group and poor prognosis group according to the 28-day prognosis. Another 202 healthy children who underwent physical examination during the same period were included as control group. ELISA was applied to measure the levels of serum MICA and CXCR1. Correlation was analyzed by Pearson's method. Multivariate Logistic regression was applied to analyze the factors influencing the prognosis of children. Receiver operating characteristic (ROC) curves were plotted to analyze the predictive value of serum MICA and CXCR1 for poor prognosis in children. Results Compared with the control group, the research group showed a decrease in CD4⁺T and CD4⁺T/CD8⁺T (P＜0.05), and an increase in CD8⁺T, and the serum MICA and CXCR1 levels (P＜0.05).The serum MICA and CXCR1 levels in children with severe pneumonia was correlated with CD4⁺T, CD8⁺T and CD4⁺T/CD8⁺T (P＜0.05). There were significant differences in the levels of CD4⁺T, CD8⁺T, CD4⁺T/CD8⁺T, MICA and CXCR1 between the poor prognosis group and the good prognosis group (P＜0.05), all of which were prognostic factors of children with severe pneumonia. The area under the curve (AUC) of combined prediction of serum MICA and CXCR1 was 0.909, which was greatly larger than that of MICA (Z=2.337, P=0.019) and CXCR1 (Z=2.555, P=0.011) alone. Conclusions Serum MICA and CXCR1 levels are increased in children with severe pneumonia, and associated with immune function and prognosis. The combination of the two has high prognostic evaluation value.

Efficacy of continuous renal replacement therapy combined with hemoperfusion in sepsis patients with acute kidney injury

TAO Ningning, WANG Haichao, SU Yueqin

2026, 46(2):  267-272.  doi:10.16352/j.issn.1001-6325.2026.02.0267

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Objective To investigate the efficacy of continuous renal replacement therapy combined with hemoperfusion in treating sepsis patients with acute kidney injury and its effect on inflammatory markers PCT, CRP and HMGB1. Methods From March 2023 to March 2024,60 patients with sepsis-induced acute kidney injury admitted to Yinchuan First People's Hospital were selected. According to the random number table method, they were divided into a control group receiving CRRT treatment and an observation group receiving CRRT combined with HP treatment, with 30 cases in each group. The sequential organ failure assessment score, levels of serum creatinine (Scr), urea nitrogen (BUN), PCT, CRP, HMGB1, acute physiology and chronic health evaluation Ⅱ score were observed in the two groups, and the 28-day mortality rate was recorded. Results Compared with the control group: after treatment, the renal function indexes Scr, BUN levels and APACHE Ⅱ scores of the observation group were significantly decreased (P＜0.05); The levels of inflammatory factors PCT, HMGB1 and IL-6 in the observation group were significantly decreased (P＜0.05). The hospitalization time of the observation group was (14.4±3.4) vs (22.5±5.3)d, the mechanical ventilation time was (9.4±2.2) vs (14.6±3.1)d, and the 28-day mortality rate in observation group was lower (3.33% vs 20.00%, P＜0.05). The overall efficacy of the observation group was better (93.33% vs 73.33%, P＜0.05). Conclusions CRRT combined with HP in treating sepsis with acute kidney injury can reduce the inflammatory response, promote the recovery of renal function, reduce the 28-day mortality rate, and improve the overall efficacy.

Relationship between peripheral blood NLRP3, IL-18, IL-1 β and the prognosis of acute exacerbation of chronic obstructive pulmonary disease

GAO Shenghu, WU Zhifei, YANG Yongbao, LI Shu

2026, 46(2):  273-277.  doi:10.16352/j.issn.1001-6325.2026.02.0273

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Objective To investigate the expression of NLRP3 mRNA in peripheral blood mononuclear cells (PBMCs) and the serum levels of interleukin-18 (IL-18) and interleukin-1β (IL-1β), as well as their clinical significance, in patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). Methods A total of 220 patients with COPD were enrolled and divided into stable group (n=122) and AECOPD group (n=98) according to the severity of the disease. AECOPD patients were divided into poor prognosis group (n=31) and good prognosis group (n=67) according to prognosis. Fifty healthy subjects were selected as control group. Baseline data were collected, RT-qPCR was used to detect NLRP3 mRNA expression, and enzyme-linked immunosorbent assay was used to determine IL-1β and IL-18 levels. Multivariate Logistic stepwise regression model was used to analyze the prognostic factors of AECOPD. Receiver operating characteristic curve (ROC) was used to analyze the efficacy of NLRP3 mRNA, IL-18 and IL-1β in predicting the poor prognosis of AECOPD. Results Compared with the control group, the levels of NLRP3 mRNA, IL-18 and IL-1β in stable group and AECOPD group were increased (P＜0.05), and those indices of AECOPD group were higher than those in stable group (P＜0.05). The disease duration, NLRP3 mRNA, IL-18 and IL-1β of poor prognosis group were higher than those of good prognosis group (P＜0.05), and the FEV₁% and FEV₁/FVC of poor prognosis group were lower than good prognosis group(P＜0.05). The disease course, NLRP3 mRNA, IL-18 and IL-1β were risk factors affecting prognosis of AECOPD. ROC results showed that NLRP3 mRNA, IL-18 and IL-1β combined predicted the poor prognosis of AECOPD with an AUC of 0.985, a sensitivity of 0.940 and a specificity of 0.968. Conclusions The expression of NLRP3 mRNA in PBMCs and the serum levels of IL-18 and IL-1β are elevated in AECOPD patients. The combined detection of these three indicators shows good predictive value for poor prognosis in AECOPD.

Mini Reviews

Advances in sodium-glucose cotransporter-2 inhibitors for improving skeletal muscle metabolism and function

SHI Jingwen, WANG Yabing, SUN Ying

2026, 46(2):  278-281.  doi:10.16352/j.issn.1001-6325.2026.02.0278

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Sodium-glucose cotransporter 2 inhibitors (SGLT2is) are guideline-recommended medications for type 2 diabetes mellitus and chronic heart failure. Increasing attention is being paid to the effects of SGLT2is on body composition, including adipose tissue and skeletal muscle, with particular emphasis on the latter. SGLT2is improve skeletal muscle function through multiple mechanisms: enhancing glucose, fatty acid, and amino acid metabolism in skeletal muscle; suppressing the expression of atrophy pathway-related molecules; and alleviating oxidative stress and inflammatory responses in skeletal muscle. Collectively, these findings provide clinicians with novel diagnostic and therapeutic perspectives for managing elderly patients with chronic diseases accompanied by skeletal muscle atrophy.

Research progress on the mechanisms of omental metastasis in gastric cancer

LONG Fangwen, ZHENG Xia, QIAN Jun, ZHANG Yifen

2026, 46(2):  282-287.  doi:10.16352/j.issn.1001-6325.2026.02.0282

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Omental metastasis is recognized as one of the most common pathways of metastasis in advanced gastric cancer and is also a key factor contributing to poor prognosis in patients with advanced gastric cancer. Research has extensively focused on various aspects concerning the mechanisms of gastric cancer omental metastasis, including the tumor microenvironment, genes, adhesion molecules, exosomes, calreticulin, and complement. These factors act on the basis of the implantation of free cancer cells in the abdominal cavity. This article reviews recent advances in understanding the mechanisms of gastric cancer omental metastasis and discusses their potential research and clinical implications.

Research progress on gut microbiota and metabolic surgery for the treatment of obesity and related metabolic diseases

ZHOU Jian, YUAN Ye

2026, 46(2):  288-292.  doi:10.16352/j.issn.1001-6325.2026.02.0288

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Obesity and its associated metabolic diseases have become significant global health challenges, with conventional therapies often limited by insufficient efficacy and high relapse rates. In recent years, metabolic surgery has emerged as a critical intervention for treating obesity and related metabolic disorders. Beyond achieving substantial weight loss, it demonstrates unique therapeutic benefits, including improvements in blood glucose levels, lipid metabolism, and reduced cardiovascular risk. Notably, metabolic surgery also alters the structure and function of the gut microbiota. These changes enhance host metabolic health by restoring intestinal barrier integrity, reducing endotoxin translocation, suppressing chronic inflammatory response, and regulating the secretion of metabolic hormones, thereby improving insulin sensitivity and energy homeostasis. Therefore, this paper provides a review of recent studies on the relationship between the intestinal microbiota and metabolic surgery in obesity and its related metabolic diseases, in order to provide new ideas for future treatment strategies.

Role of Notch signaling pathway in bronchial asthma

CHEN Menglei, CUI Yun

2026, 46(2):  293-297.  doi:10.16352/j.issn.1001-6325.2026.02.0293

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The Notch signaling pathway is a critical cellular signaling pathway closely associated with physiological processes such as cell proliferation, differentiation, and apoptosis. Its aberrant activation contributes to the pathological progression of asthma through multiple mechanisms. In terms of airway inflammation, the Notch signaling pathway exacerbates T lymphocyte imbalance, leading to excessive release of pro-inflammatory cytokines. Regarding airway hyperresponsiveness, it enhances airway smooth muscle sensitivity and mucus hypersecretion by upregulating tumor necrosis factor-α (TNF-α) expression and promoting mucin MUC5AC secretion. In the context of airway remodeling, the Notch signaling pathway facilitates the loss of multiciliated cells while simultaneously increasing MUC5AC expression and secretion. Targeted intervention strategies, including γ-secretase inhibitors, mesenchymal stem cells, and active components of traditional Chinese medicine, have demonstrated potential in alleviating asthma symptoms by modulating the Notch pathway. These findings not only deepen the understanding of asthma pathogenesis but also provide a theoretical foundation for developing novel targeted therapies.

Medical Education

Exploration and practice of effective training pathways for empowering medical education with artificial intelligence

LI Hongling, ZHANG Yunzhu, HUO Qianhe, GUO Lei, PENG Yihong, WANG Jing, GUO Hengyi

2026, 46(2):  298-302.  doi:10.16352/j.issn.1001-6325.2026.02.0298

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Objective To explore effective training pathways improving teachers′ cognition of artificial intelligence(AI) and rapidly enhance their ability to apply AI in medical education. Methods A baseline questionnaire was conducted among teachers at the School of Basic Medical Sciences of Peking Union Medical College to assess their current understanding of AI-enabled medical education, acceptance, skill level and training needs. Based on the analysis, a cyclic enhancement training model (“Cognition Guidance-Skill Instruction- Output Motivation- Practice Validation”) was developed. A follow-up questionnaire was used to comprehensively assess the training outcomes. It encompassed basic information, training participation, effectiveness and satisfaction evaluation,and outcome assessment. Results The proportion of teachers with insufficient AI understanding dropped from 66.66% to 29.27%. Eighty-five percent rated the training as highly or very targeted and effective; over 90% reported clear theoretical explanations and strong practical inspiration. Overall satisfaction (satisfied/very satisfied) was 90.24%, 80.49% confirmed a significant improvement in AI application competencies, and 97.56% expressed expectation for future training. Conclusions The cyclic enhancement training model effectively improves teachers′ cognition of AI integration into medical education and rapidly enhances their proficiency in applying AI tools to teaching practices.

Continuing education for ultrasound physicians:current challenges and strategic development

JIANG Jie, ZHANG Qi, LIU Chang, ZHAO Bo, SUN Yan, JIANG Ling

2026, 46(2):  303-306.  doi:10.16352/j.issn.1001-6325.2026.02.0303

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Objective To comprehensively investigate the current situation of ultrasound refresher trainee and propose evidence-based strategies for optimizing the continuing medical education (CME) system for sonographers, so as to promote a balanced workforce and improve overall service capacity. Methods A structured questionnaire was distributed to 1 420 ultrasound refresher trainees to collect data on gender, workplace, hospital grade, education and learning experience, professional title and other demographic characteristics; all data were analyzed descriptively. Results The number of trainees increased year by year, with females comprising the large majority. Trainees were distributed in an “inverted-pyramid” pattern: 56.2% came from tertiary A-level hospitals, whereas only 7.3% were from primary-level institutions. Geographically, North and East China were over-represented, while Northwest and South China were under-represented. The majority of participants held a bachelor's degree and an intermediate professional title. Conclusions There is a notable concentration of ultrasound physician training resources in specific institutions and regions in China, with physicians in primary care and remote areas having significantly fewer opportunities to access high-quality training.

Medical Supervision

Unplanned massive transfusion as a quality evaluation indicator for clinical blood safety management

SUN Shaohua, ZHANG Guozong, SHAN Kai

2026, 46(2):  307-310.  doi:10.16352/j.issn.1001-6325.2026.02.0307

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Objective To explore the practical value of using unplanned massive transfusion as a quality evaluation indicator in clinical blood use management. Methods A before and after study design was employed to establish a scientific cycle of “assessment-intervention-reassessment.” Using the clinical blood usage records of Beijing Tiantan Hospital, Capital Medical University, from 2023 to 2024, we systematically collected all cases of unplanned massive transfusion as study subjects. A controlled study was conducted, with cases from 2023 serving as the baseline control group (pre-intervention) and cases from 2024 as the intervention group. Data from both groups were analyzed to evaluate the effects of implementing “unplanned massive transfusion” as a key quality indicator on reducing total blood consumption, optimizing transfusion processes, and decreasing the incidence of adverse events. Results Following the implementation of improvement measures—including adopting unplanned massive transfusion as a quality indicator, strengthening pre-operative assessment and approval, and enhancing training and assessment for medical staff in 2024—a positive outcome was recorded even an increase in both the total number of surgeries and their complexity during this period. The number of massive transfusion cases decreased by 31.7% (71 vs. 104), the number of unplanned massive transfusion cases decreased by 37.5% (45 vs. 72). Overall blood consumption was reduced by 10.9%. Conclusions Application of unplanned massive transfusion as a quality evaluation indicator for continuous improvement in clinical blood use management is feasible and can enhance both quality and efficiency of blood transfusion management in hospitals.