Table of Content

05 March 2026, Volume 46 Issue 3

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Original Articles

Icariin treats for psoriasis of mouse models through inhibition of PI3K-AKT-vascular proliferation pathway

LIN Qing, YANG Bin, ZHU Rongjia, ZHAO Chunhua, SONG Ping

2026, 46(3):  311-316.  doi:10.16352/j.issn.1001-6325.2026.03.0311

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Objective To explore the mechanism of icariin (ICA) in the treatment of psoriasis. Methods Thirty-six C57BL/6 mice were randomly divided into 6 groups with 6 in each: a blank(Ctrl) group, a model group, a positive control group treated with methotrexate, and experimental groups treated respectively with low, medium, and high doses of ICA. Ann imiquimod (IMQ)-induced psoriasis animal model was established. Methotrexate was given by intragastric administration at a concentration of 1 mg/kg. The animals in low, medium, and high dose ICA groups received intragastric administration of 0.4 mg/100 mL, 0.8 g/100 mL and 1.2 g/100 mL respectively. On day 6 of the experiment, dorsal skin samples were collected from all six groups of mice for Hematoxylin-Eosin (HE) staining microscopy. RT-qPCR was used to measure the inflammatory level of Il-6, Il-17a and Tnf-α in the mouse skin. Immunofluorescence double staining was employed to observe CD31 and VEGF level in the mouse skin. Western blot was used to detect the protein level of PI3K, AKT, p-PI3K, and p-AKT in the mouse skin. Results Compared with the model group, the high-dose ICA group significantly improved IMQ-induced skin thickening(P＜0.000 1) and reduced the PASI score in mice. The high-dose ICA group significantly decreased mRNA level of Tnf-α, Il-6 and Il-17a in the skin of psoriasis mice (P＜0.000 1) and reduced the level of CD31 and VEGF in the skin of psoriasis mice. Additionally, the high-dose ICA group reduced protein level of PI3K(P＜0.05), AKT(P＜0.05), p-PI3K (P＜0.05) and p-AKT (P＜0.01) in the mouse skin. Conclusions High-dose 1.2 g/100 mL ICA exhibits superior anti-psoriatic properties, with its mechanism potentially involving inhibition of PI3K-AKT-mediated angiogenesis.

Urinary proteome in aging mouse models reflects changes in the cerebral cortex

HE Mengzhen, ZHANG Yuxue, LIU Tingting, HU Siqi, LI Jun, SUN Wei

2026, 46(3):  317-324.  doi:10.16352/j.issn.1001-6325.2026.03.0317

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Objective To detect the proteomic changes in cerebral cortex and urine of aging mice and to explore the correlation between urinary and cerebral cortical proteomes. Methods Six mice of 1, 6 and 18-month-old were collec-ted, urine was collected and tissue was isolated from cerebral cortex under physiological conditions. Proteomic analysis was performed by liquid chromatography-tandem mass spectrometry(LC-MS/MS) was used to find potential differences and to analyze the function and the association between urine component and cerebral cortex proteomes. Results A total of 13 021 protein components were identified in the cerebral cortex and 1 064 protein components were identified in urine of mice. One-month-old mice proteomes focused on growth and development-related pathways, 6-month-old mice proteomes focused on energy metabolism and other pathways, and 18-month-old mice proteomes exhibited metabolic abnormalities and homeostatic imbalances. Correlation analysis revealed that urine can reflect the changes in proteins related to immunity, cell proliferation and aging in the cerebral cortex. Conclusions Urine proteome of senescent mice reflects cerebral cortex changes and provides clues for research on bio-markers of aging-related diseases.

Piezoelectric-responsive hydrogel promotes matrix synthesis in nucleus pulposus cells of rats

GUAN Yunbo, ZHAO Ziteng, ZHANG Ziqiang, SUN Xiaofei, ZHAO Yantao, WANG Zuqiang

2026, 46(3):  325-331.  doi:10.16352/j.issn.1001-6325.2026.03.0325

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Objective To investigate the property of fundamental material properties of a piezoelectic-responsive hydrogel (KNN/GelMA), including its mechanical, piezoelectric and biocompatibility characteristics, and to examine the effects of its piezoelectric response the synthetic metabolism of nucleus pulposus cells (NPCs). Methods 1)Material characterisation: KNN was uniformly dispersed in GelMA hydrogel via ultrasonication to prepare a photopolymerisable, degradable piezoelectric hydrogel. Preliminary physicochemical characterisation was conducted by measuring microstructure, piezoelectric properties and so on. 2) Cellular experiments: The piezoelectic-responsive hydrogel was co-incubated with rat primary NPCs. The proliferation capacity and biocompatibility were assessed using the CCK-8 methods and a dead/live staining kit. Gene expression related to extra cellular matrix synthesis was detected by RT-qPCR. Results The material surface exhibited a uniform pore structure, with KNN nanoparticles distributed evenly throughout the hydrogel. Piezoelectric output experiments demonstrated significant voltage and current generation under applied force(P＜0.05). The proliferation of cells in the 0.4% w/v KNN/GelMA group was significantly enhanced over time as compared with that in 0.2% w/v KNN/GelMA group, and live cells (green) were dominant(P＜0.05). RT-qPCR showed that the mRNA levels of related aggrecan(Acan) and type Ⅱ collagen (Col2) in the extra cellular matrix of chondrocytes in the TNF-α + KNN/GelMA + ultrasound(US) group was lower than those in the TNF-α + KNN/GelM group(P＜0.05). Conclusions A light-curable, degradable, piezoelectric-responsive hydrogel which exhibits a uniform porous structure has developed. It has a significant piezoelectric effect, excellent biocompatibility, and can significantly promote the cell matrix synthesis ability of nucleus pulposus cells. It is a promising material option for repairing degenerative disc injuries.

Absolute quantification of plasma IgG N-glycopeptides as a biomarker for diagnosis of the early COPD

LIU Zhaoyi, YIN Meiling, WANG Lin, ZHOU Jinyu

2026, 46(3):  332-338.  doi:10.16352/j.issn.1001-6325.2026.03.0332

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Objective To investigate the potential of the absolute quantifaction of plasma IgG N-glycopeptides for the early diagnosis of chronic obstructive pulmonary disease (COPD). Methods Research objects were randomly selected from the healthy control (HC) group, the early COPD (ECOPD) group and the stable COPD(COPD) group from previous research cohort(20 cases for each group), and targeted differential glycopeptides were selected based on the previously obtained relative quantitative data of plasma IgG N-glycopeptides. Absolute concentration of glycopeptide was measured with internal standard method. The linear relationship between the absolute concentra- tion of the targeted glycopeptides and the ratio of forced expiratory volume in one second to forced vital capacity (FEV1/FVC) was analyzed. The receiver operating characteristic (ROC) curves were generated to compare the diagnostic efficacy of individual glycopeptides indicators, age, smoking index and their combination. Results The relative quantification showed that the plasma level of IgG2 G2FS glycopeptides was significantly higher in the HC group than that in the ECOPD and COPD groups (P＜0.05). The absolute quantification further clarified a successive decrease in its concentration across the HC, ECOPD, and COPD groups, with a particular difference between the HC and COPD groups (P＜0.001). ROC analysis indicated that the diagnostic efficacy of the plasma IgG2 G2FS concentration for ECOPD (area under curve,AUC=0.765) was superior to that of age (AUC=0.624) or smoking index (AUC=0.602). However, the combined model incorporating IgG2 G2FS, age, and smoking index (AUC=0.780) showed comparable performance to IgG2 G2FS alone. Conclusions The absolute concentration of plasma IgG2 G2FS exhibits competitive diagnostic value for early COPD, suggesting plasma IgG2 G2FS is a potential biomarker for early digestion of COPD.

Nlrp3^T346M mutant transgenic mice present abnormal circadian entrainment and affect liver inflammatory injury

WANG Yuxin, YANG Mei, CHEN Quanlin, ZHU Lei

2026, 46(3):  339-344.  doi:10.16352/j.issn.1001-6325.2026.03.0339

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Objective To explore the potential mechanism by which NLRP3 mutation leads to its sustained activation and subsequent liver injury at the transcriptome level with an animal model of Nlrp3^T346M mutant transgenic mice. Methods Liver tissues from Nlrp3^T346M mice and their wild type (WT) littermates were subjected to transcriptome sequencing. Gene expression difference between the two groups was analyzed, followed by GO and KEGG enrichment analyses of the differentially expressed genes (DEGs). RT-qPCR was performed to verify the expression of relevant DEGs. Results Compared with WT group, a total of 258 DEGs were screened in the livers of Nlrp3^T346M mice, of which 197 were up-regulated and 61 were down-regulated. Enrichment analysis showed that the DEGs were mainly involved in circadian entrainment, as well as metabolic pathways of steroids, retinol and olefinic compounds,etc. RT-qPCR results showed mRNA expression trends of key DEGs in the circadian entrainment pathway, namely Cacna1h,Camk2b,Gnai1,Mtnr1a and Nos1ap were consistent with those observed in the transcriptome sequencing. Conclusions Sustained activation of NLRP3 in the liver tissue of Nlrp3^T346M mice may interfere with circadian entrainment, which in turn disrupts temporal regulation of downstream metabolism and hormone secretion, thus leads to liver injury.

Aging of NK cells mediates the contradictory phenotype of “high inflammation and weak anti-infection” in dermatomyositis patients

REN Leilei, LYU Yulin, WANG Haohua, ZHANG Wanjun, MENG Shu, JIANG Minghong

2026, 46(3):  345-351.  doi:10.16352/j.issn.1001-6325.2026.03.0345

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Objective To explore the intrinsic mechanism of the contradictory phenotype “high inflammation and weak anti-infection” in MDA5 antibody-positive in patients with dermatomyositis (MDA5⁺ DM), and to clarify the senescent characteristics and functional status of peripheral blood natural killer (NK) cells, thus provide experi- mental basis for developing new DM therapeutic strategy. Methods Single-cell RNA sequencing (scRNA-seq) was used to analyze the Senescence-Associated Secretory Phenotype (SASP) score and function-related differential genes of peripheral blood NK cells in 6 MDA5⁺ DM patients and 2 healthy controls (HC). Peripheral blood was collected from 83 patients (38 in active phase, 45 in stable phase) and 44 HCs. C12FDG staining combined with flow cytometry was performed to detect the senescent phenotype of NK cells. The secretion level of interferon-γ(IFN-γ) and granzyme B (GZMB) in NK cells were measured under basal conditions and after IL-12/IL-15/IL-18 stimulation. Spearman correlation analysis was applied to evaluate the association between NK cell senescence degree and function. Results ScRNA-seq showed that the SASP score of NK cells in DM patients was significantly higher than that in HC(P＜0.001). The mean fluorescence intensity (MFI) of C12FDG in peripheral blood NK cells of DM patients in both active and stable phases was significantly higher than that in HCs(P＜0.05 and P＜0.001, respectively), with no significant difference between different disease stages. Functional tests revealed that the basal secretion level of IFN-γ and GZMB in DM patients' NK cells were significantly higher than those in HCs (P＜0.01 or P＜0.000 1). Incubation with IL-12/IL-15/IL-18, reduced IFN-γ secretion level and inhibited its increase in DM patients' NK cells as compared to the situation in HCs (P＜0.05 or P＜0.000 1), while GZMB secretion remained at a high level, and like HCs, it showed almost no response to cytokines. Correlation analysis suggested a moderate negative correlation between NK cell C12FDG accumulation and IFN-γ stress response ability (r=-0.398 1, P=0.002 9). Conclusions dPeripheral blood NKf cells in DM patients show obvious senescent characteristics, which are closely related to the defective stress response of IFN-γ secretion. This may contribute to the formation of the “high inflammation and weak anti-infection” contradictory phenotype in DM patients. This result provides experimental basis for developing therapeutic strategies targeting at NK cell senescence and for identification of related biomarkers in DM patients.

Knock-down MALAT1 reduces ox-LDL- induced-inflammation and cell damage of macrophages

SONG Ning, LUO Junyi, JI Wei, LI Yanhong, LI Xiaomei, YANG Yining

2026, 46(3):  352-358.  doi:10.16352/j.issn.1001-6325.2026.03.0352

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Objective To explore the role and potential mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in inflammatory response and cell damage of macrophages induced by oxidized low density lipoprotein (ox-LDL). Methods THP-1 cells were induced to differentiate into macrophages by phorbol ester(PMA). Macrophages were co-cultured with ox-LDL to construct a cell injury model. Lipid accumulation was observed by Oil Red O staining microscopy. MALAT1 was knocked down by transfection of shRNA. The experimental group included control group, ox-LDL group, ox-LDL+shNC group and ox-LDL+shMALAT1 group. Total cholesterol and triglyceride in cells were measured. Apoptosis was detected by flow cytometry. The level of IL-6, TNFα and MCP-1 were detected by ELISA. The expression of NLRP3, RIPK1, caspase-8, p65 and SR-A was detected by RT-qPCR and Western blot. Results Compared with the control group, the cell lipid accumulation, total cholesterol and triglyceride contents, cell apoptosis, IL-6, TNFα and MCP-1 levels and the expression of NLRP3, RIPK1, caspase-8, p-p65 and SR-A increased significantly in ox-LDL group(P＜0.05). Compared with ox-LDL group, ox-LDL+shMALAT1 group the contents of total cholesterol and triglyceride, apoptosis, IL-6, TNFα and MCP-1, and the expression of NLRP3, RIPK1, caspase-8, p-p65 and SR-A all significantly decreased(P＜0.05). Conclusions MALAT1 may play an important role in ox-LDL-induced cell injury by regulating NLRP3 inflammatory corpuscles and related signal pathways. Knockdown of MALAT1 can significantly reduce the inflammatory reaction and cell damage induced by ox-LDL, which provides a potential target for the treatment of atherosclerosis.

D-pinitol alleviates brain injury in rat models with cerebral ischemia-reperfusion

XU Boxin, SHAN Yuan, YANG Yunpeng

2026, 46(3):  359-366.  doi:10.16352/j.issn.1001-6325.2026.03.0359

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Objective To investigate the therapeutic effects of D-pinitol (DP) on rats with cerebral ischemia-reperfusion injury (CI/RI). Methods Rats were randomly divided into 6 groups with 12 in each: sham group (sham), model group (CI/RI rat model established by the modified Longa suture method), low (L-DP), medium (M-DP), and high-dose DP group (H-DP) (gavaged with 10, 20, or 40 mg/kg DP, respectively) and H-DP+inhibitor group (inhibitor, gavaged with 40 mg/kg DP and intraperitoneally injected with 30 mg/kg Nrf2 inhibitor ML385). Zea Longa score were evaluated using a double-blind method, cerebral infarction volume was assessed by TTC staining, neuronal morphology was observed via hematoxylin-eosin (HE) and Nissl staining microcopy, apoptotic cells were labeled by TUNEL staining. The activity of SOD and the contents of GSH, MDA, TNF-α, IL-1β and IL-6 in brain tissues were detected by commercial kits, Fe²⁺ content in brain homogenates was measured by visible spectrophotometer. mRNA levels of heme oxygenase-1 (HO-1), NAD (P) H quinone dehydrogenase 1 (NQO1), and glutathione peroxidase 4(GPX4) were analyzed by RT-qPCR. Protein expression of nuclear Nrf2, Keap1, HO-1, NQO1, and GPX4 in brain tissues was detected by Western blot. Results Compared with sham group, the brain injury of rats in the model group showed significant brain injury, and the neurological function score, cerebral infarction volume and the proportion of TUNEL⁺ cells were increased (P＜0.05) while GSH content and SOD activity decreased (P＜0.05). The level of MDA, TNF-α, IL-1β, IL-6 and Fe²⁺ increased (P＜0.05). The protein level of GPX4, Nrf2 (nucleus), HO-1 and NQO-1 decreased (P＜0.05), while the protein level of Keap1 increased(P＜0.05). Compared with model group, the brain injury of rats in L-DP, M-DP and H-DP group was significantly alleviated. The neurological function score, cerebral infarction volume and the proportion of TUNEL⁺ cells were all decreased (P＜0.05). The GSH content and SOD activity increased (P＜0.05), while the levels of MDA, TNF-α, IL-1β, IL-6 and Fe²⁺ all decreased (P＜0.05). The protein levels of GPX4, Nrf2 (nucleus), HO-1 and NQO-1 increased (P＜0.05), while the protein level of Keap1 decreased (P＜0.05). Compared with H-DP group, the brain injury of rats in the inhibitor group was aggravated, and the neurological function score, cerebral infarction volume and the proportion of TUNEL⁺ cells were all increased (P＜0.05). The GSH content and SOD activity decreased (P＜0.05), while the level of MDA, TNF-α, IL-1β, IL-6 and Fe²⁺ all increased(P＜0.05). The protein level of GPX4, Nrf2 (nucleus), HO-1 and NQO-1 decreased (P＜0.05), while the protein level of Keap1 increased (P＜0.05). Conclusions D-pinitol alleviates brain injury in CI/RI rats through anti-oxidation, anti-inflammation, anti-apoptosis effects and inhibition of ferroptosis.

Therapeutic effects of Sofren injection on non-alcoholic fatty liver disease in rat models

XU Xia, WANG Fubing, ZHAO Peipei, FAN Hui, LI Xin, ZHANG Gu, GU Xinhong

2026, 46(3):  367-373.  doi:10.16352/j.issn.1001-6325.2026.03.0367

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Objective To investigate the hepato-protective effects of Sorfren injection on rat liver injury resulted from non-alcoholic fatty liver disease (NAFLD). Methods Rats were randomly divided into control, NAFLD model and Sofren-treated groups. The Sofren-treated groups was developed by feeding a high-fat diet (HFD) for 8 weeks. Subsequently, the Sofren-treated group received tail vein injections of Sofren solution (0.4 mL/100 g) for 8 weeks. Serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were measured using an automatic biochemical analyzer. Tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β),IL-6 and malondialdehyde (MDA) were quantified by enzyme-linkedimmunosorbent assay(ELISA). Superoxide dismutase (SOD) activity was assessed by chromogenic method. Histopathological evaluations were performed by Hematoxylin-Eosin (HE) and Prussian blue staining. Immunohistochemistry and Western blot were applied to analyze the expression of glutathione peroxidase 4 (GPX4), nuclear factor erythroid 2-related factor 2 (Nrf2),heme oxygenase-1 (HO-1), transferrin receptor 1 (TFR1) and ferritin heavy chain 1 (FTH1). Results Compared with control group, the model group exhibited significant elevation of serum ALT, AST, MDA, and inflammatory mediators (TNF-α, IL-1β, IL-6), reduction of SOD activity, increased hepatic iron deposition, down-regulated Nrf2, HO-1, and GPX4 expression, and up-regulated level of TFR1 and FTH1(P＜0.05). Treatment with Sofren injection markedly reversed these pathological alterations(P＜0.05). Conclusions Sofren injection may alleviate liver injury in NAFLD rats.

Elevated expression of circGAPVD1 in plasma-derived exosomes is correlated with disease progression in colorectal cancer patients

ZHAN Sen, LIU Yujie, LI Tiankang, ZHANG Chong, REN Zeqiang, ZHANG Yi

2026, 46(3):  374-380.  doi:10.16352/j.issn.1001-6325.2026.03.0374

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Objective To explore the differential expression of circGAPVD1 derived from plasma exosomes in patients with colorectal cancer (CRC), and to analyze its potential as a diagnostic marker for colorectal cancer. Methods A total of 111 CRC patients who underwent surgical treatment and were pathologically confirmed at the Affiliated Hospital of Xuzhou Medical University from January 2022 to August 2023 were enrolled, along with 85 healthy individuals from routine physical examinations as controls. Plasma exosomes were isolated and characterized using transmission electron microscopy (TEM), Western blot and nano-particle size analysis. The expression level of circGAPVD1 was detected by RT-qPCR. Receiver operating characteristic (ROC) curve analysis was performed to evaluate the diagnostic efficacy of circGAPVD1 for CRC. Results Compared with healthy controls, circGAPVD1 was significantly expressed higher in the plasma exosomes of patients with CRC(P＜0.01). The sensitivity of circGAPVD1 in the diagnosis was 77.5% with specificity as 76.5%. The area under ROC curve was 0.818 6,suggesting circGAPVD1 has robust diagnostic efficacy for CRC. In addition, related to the pathological data of patients with CRC, the lymph node metastasis and TNM staging showed a positive relation to high expression of circGAPVD1. Conclusions Plasma exosome-derived circGAPVD1 is a potential novel biomarker which support the clinical diagnosis of CRC.

Circulating microparticles from acute coronary syndrome patients complicated with type 2 diabetes induce endothelial cell injury in rats

CHANG Fengjun, WANG Xing, YANG Yujuan, LI Hongwen

2026, 46(3):  381-387.  doi:10.16352/j.issn.1001-6325.2026.03.0381

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Objective To investigate the effects of circulating microparticulates (MPs) on vascular endothelium injury in patients with acute coronary syndrome (ACS) and type 2 diabetes (T2DM). Methods MPs were extracted from control (n=15), ACS patients (ACS, n=18), T2DM patients (T2DM, n=18) and ACS patients with T2DM (ACS+T2DM group, n=18). After incubation of rat thoracic artery tissue with MPs, the effects of MPs on endothelial dependent vasodilatation was detected with biological assay, expression of caveolin-1, coupling of endothelial nitric oxide synthase (eNOS) with heat shock protein 90 (Hsp90) was detected with Western blot. The changes in nitric oxide (NO) and superoxide anion were examined with chemical assay. Results The MPs concentration in ACS+T2DM patients samples was higher than that in control (P＜0.05). However, compared with ACS and T2DM patients, there was no statistically significant difference in MPs concentration. Compared with the control, regardless of ACS, T2DM and ACS+T2DM, their MPs inhibited endothelial dependent vasodilatation function, eNOS and Hsp90 coupling and NO production and stimulated expression of caveolin-1 and generation(P＜0.05). However, compared with ACS and T2DM patients, the effects of MPs were stronger in ACS+T2DM(P＜0.05). Conclusions The changes in the quality (or function) of MPs in ACS+T2DM lead to damage of rat vascular endothelium by MPs. MPs are potential marker molecules to support diagnosis of endothelial dysfunction.

Nicodil preconditioning improves cardiac function in rat models of diabeties complicated with coronary heart disease

BIAN Ya, GUO Jie, CAO Weiguang, LYU Xiaomian

2026, 46(3):  388-395.  doi:10.16352/j.issn.1001-6325.2026.03.0388

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Objective To identify the impacts of nicorandil (Nic) on cardiac function of rats with diabetes mellitus and coronary heart disease (DM/CHD) and to explore the potential mechanism. Methods Rats were divided into: control group, DM/CHD group, DM/CHD+Nic group and DM/CHD+Nic+shTRPV1 group. The cardiac function parameters were detected by electrocardiogram. Blood was collected for biochemical index detection. Cardiac histo-pathological changes, collagen deposition and apoptosis were determined by HE, Masson trichrome and TUNEL staining microcopy respectively. The protein expression was analyzed by Western blot. Results In comparation to control group, the cardiomyocyte diameter and collagen accumulation were increased (P＜0.05). Apoptotic cells and the expression of Bax and cleaved caspase-3 were increased (P＜0.05),expression of Bcl-2, TRPV1, p-PI3K and p-Akt was decreased. Compared with DM/CHD group, myocardial cell diameter and collagen accumulation were reduced (P＜0.05). Apoptotic cells and the level of Bax and cleaved caspase-3 were reduced (P＜0.05).The expression of Bcl-2, TRPV1, p-PI3K and p-Akt was enhanced (P＜0.05). Compared with DM/CHD+Nic group, myocardial cell diameter and collagen accumulation were increased (P＜0.05). Apoptotic cells and the expression of Bax and cleaved caspase-3 were up-regulated (P＜0.05).The expression of Bcl-2, TRPV1, p-PI3K and p-Akt was down-regulated. Conclusions Nic improves cardiac function in DM/CHD rats with potential mechanism of regulating TRPV1-PI3K/Akt signaling pathway.

Over-expression of Vps16 improves myocardial function in rats with myocardial ischemia-reperfusion

WANG Yangui, TAN Jinghua, ZHAO Jin, WANG Tao, MA Tingting, SHAO Lili, QI Weigang

2026, 46(3):  396-401.  doi:10.16352/j.issn.1001-6325.2026.03.0396

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Objective To investigate the role of vacuolar sorting protein 16 (Vps16) in myocardial ischemia-reperfusion (MI/R) injury in rats. Methods The rats were randomly divided into sham group, MI/R group, lentivirus blank vector (Lv-NC) group and lentivirus overexpressing Vps16 (Lv-Vps16) group, with 6 rats in each group. Left ventricular function was measured by echocardiography, including LVIDd and LVISd. LVFS and LVEF were calculated. ELISA was used to detect the levels of serum myocardial injury markers (CK-MB, cTnⅠ and LDH) and inflammatory factors (IL-6, TNF-α, and IL-1β). HE and TUNEL staining were employed to assess myocardial injury and apoptosis, while immunohistochemistry (IHC) and Western blot were used to determine the expression levels of Vps16, UV radiation-associated gene protein (UVRAG), Ras-associated protein 7 (Rab7), and autophagy- related proteins. Results Compared with the sham group, LVIDd, LVISd, CK-MB, cTnⅠ and LDH, the rate of TUNEL-positive cells and the levels of IL-6, TNF-α, IL-1β and p62 in the MI/R group were increased. LVFS, LVEF, Vps16, LC3Ⅱ/LC3Ⅰ, UVRAG, and Rab7 proteins were down-regulated (all P＜0.05). The myocardial tissue structure of MI/R group was disordered, indicating that the MI/R model was successfully constructed. Over-expression of Vps16 alleviated myocardial injury and inflammatory response, and improved cardiac function in rats. Conclusions Vps16 can alleviate MI/R injury by activating the UVRAG/Rab7 signaling to induce cardiomyocyte autophagy.

Discriminant analysis on influencing factors of hope level in patients with lung cancer based on decision tree and Logistic regression models

LYU Juan, JI Shuo, LIU Ya, SUN Wen, PAN Ruili

2026, 46(3):  402-410.  doi:10.16352/j.issn.1001-6325.2026.03.0402

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Objective To identify influencing factors of hope level in patients with lung cancer, so as to find and identify patients with lower hope level as early as possible, and to provide reference for the formulation of intervention measures to improve hope level in patients with lung cancer. Methods Total of 266 patients with lung cancer who were treated in Peking Union Medical College Hospital from July 2024 to December 2024 were selected as the research objects. Herth Hope Index (HHI) was used to investigate the hope level of the included patients.The hope level of lung cancer patients with different characteristics was compared, and the decision tree(DT) and Logistic regression model were used to analyze the influencing factors of the hope level of lung cancer patients. Results After excluding 9 patients who answered invalid questionnaires, 257 patients were included in this study. Logistic regression model showed that the days since diagnosis (B=-0.001), lung cancer classification[adenocarcinoma(B=0.177), squamous cell carcinoma (B=1.949), others (B=1.458)], education level [high school, vocational school or technical school (B=-1.182), junior college (B=0.392), bachelor′s degree or above (B=1.040)], immunotherapy(B=-0.682), the score of Eastern Cooperative Oncology Group (ECOG) performance status (PS) [grade 1 (B=1.657), grade 2 (B=2.102) , grade 3 (B=0.171)]and the score of Connor-Davidson Resilience Scale (CD-RISC) (B=-0.060) were independent factors influencing the occurrence of the medium hope level in lung cancer patients.The results of decision tree showed that the total score of CD-RISC was the main factor affecting the hope level of lung cancer patients, followed by education level and the days of diagnosis. The area under the curve(AUC) of the two models was 0.853(0.806,0.900) and 0.850 (0.801, 0.898) respectively with no statistically significant difference (Z=0.144, P=0.885). Conclusions Both Logistic regression model and decision tree have certain application value in predicting the hope level of lung cancer patients. It is suggested to combine the two models in clinical practice in order to improve the hope level of lung cancer patients.

Expressions of testicular receptor 4 protein and cluster of differentiation 36 (CD36) in the mucosa of tracheobronchial tuberculosis at different stages

LUO Linzi, LUO Li, ZHOU Lei, LU Zhibin, DING Yan, XIAO Yangbao

2026, 46(3):  411-416.  doi:10.16352/j.issn.1001-6325.2026.03.0411

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Objective To clarify whether testicular receptor 4(TR4) protein and cluster of differentiation 36(CD36) protein are involved in the formation of tracheobronchial mucosal lesions of tracheobronchial tuberculosis (TBTB). Methods Tissues of tracheobronchial mucosal lesions of TBTB patients were collected and divided into 2 groups: active stage group and inactive stage group. The normal bronchial mucosa tissues were collected as control group. The expressions of TR4 and CD36 in 3 groups were detected by immune histochemistry and Western blot. The percentages of macrophage and foamy macrophage was detected by flow cytometry. Results The expression level of TR4 was as follows: active stage ＞ inactive stage and control group(P＜0.01). The expression level of CD36 was as follows: active stage ＞ control group ＞ inactive stage(P＜0.05). The percentages of macrophage and foamy macrophage were as follows: active stage ＞ inactive stage and control group(P＜0.05). Conclusions TR4 and CD36 seemed to play some roles in the formation of tracheobronchial mucosal lesions in active TBTB trachea the formation of foamy macrophage.

Clinical Sciences

Value of serum D-dimer in evaluating chemotherapy effect and prognosis in patients with non-small cell lung cancer

ZHANG Zhen, YANG Lianren, HU Junkun, ZHANG Wei, LIANG Wei

2026, 46(3):  417-420.  doi:10.16352/j.issn.1001-6325.2026.03.0417

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Objective To investigate the value of serum D-dimer in evaluating chemotherapy effect and prognosis in patients with non-small cell lung cancer(NSCLC). Methods A total of 60 patients with NSCLC were collected from June 2022 to December 2023. They were divided into effective group (n=45) and ineffective group (n=15) according to the difference of chemotherapy effect. Serum D-dimer levels was measured by immunoturbidimetry and was then compared between the two groups. The efficacy of the above indexes in predicting chemotherapy effect was analyzed by receiver operating characteristic (ROC) curve. In addition, patients were divided into good prognosis group (n=40) and bad prognosis group (n=20) according to their prognosis. Univariate and multivariate analysis was used to determine the factors affecting the prognosis of NSCLC patients. Results The serum D-dimer level in the ineffective group was (1.30±0.42) mg/L, which was higher than that in the effective group (0.97±0.32)mg/L(t=3.192, P＜0.01). ROC curve analysis confirmed that the area under the curve(AUC) of serum D-dimer level to predict chemotherapy failure in NSCLC patients was 0.760, the sensitivity was 0.667 and the specificity was 0.711. The Joden index was 0.356, the optimal threshold was 1.16 mg/L, and the 95% CI was 0.631-0.889. Univariate analysis showed that TNM stage, differentiation degree of the cancer cells, lymph node metastasis and serum D-dimer level were related to the prognosis of patients with NSCLC (all P＜0.05). Multivariate Logistic regression analysis showed that the risk factors for poor prognosis in NSCLC patients included the TNM stage Ⅳ; Low differentiation; Lymph node metastasis and serum D-dimer (all OR＞1, P＜0.05). Conclusions Serum D-dimer can provide reliable evidence to the evaluation of chemotherapy effect and prognosis of NSCLC patients.

Diagnostic value of serum level of Gal-3, VASH-1 and NGAL for early renal dysfunction in women with gestational diabetes mellitus

WANG Qianchen, SHI Xingchi, ZHENG Weiying

2026, 46(3):  421-426.  doi:10.16352/j.issn.1001-6325.2026.03.0421

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Objective To explore the diagnostic value of serum galectin-3 (Gal-3), vasohibin-1 (VASH-1) and neutrophil gelatinase associated lipocalin (NGAL) for early diagnosis of renal dysfunction in women with gestational diabetes mellitus (GDM). Methods A total of 96 GDM patients admitted to Jinhua People′s Hospital of Zhejiang Province from June 2023 to July 2024 were selected as the observation group, and 96 pregnant women with normal prenatal examination during the same period were selected as the control group. ELISA method was used to detect the serum level of Gal-3, VASH-1 and NGAL. According to the content of albumin in the urine of the patients at 24 h, the observation group was divided into diabetic nephropathy group and diabetic group. Pearson method to analyze correlations; Logistic regression analysis of related factors; ROC curves were used to predict performance. Results Glycosylated hemoglobin, low-density lipoprotein, high-density lipoprotein and fasting blood glucose level in patients with gestational diabetes and the serum level of Gal-3, VASH-1 and NGAL in patients with gestational diabetes mellitus were higher than those in the control group(P＜0.05). The serum level of Gal-3 and VASH-1, was positively correlated , serum level of Gal-3 and NGAL, serum level of VASH-1 and NGAL were all positively correlated (P＜0.001). The level of fasting blood glucose, serum Gal-3, VASH-1 and NGAL in the diabetic nephropathy group were significantly higher than those in the diabetic group (P＜0.05). High level of serum Gal-3, VASH-1 and NGAL were independent risk factors for early renal impairment in patients with GDM(P＜0.05). The serum level of Gal-3, VASH-1 and NGAL and the area under the curve (AUC) of the combined prediction of early renal impairment in patients were 0.853, 0.678, 0.865 and 0.955, respectively. Conclusions The serum level of Gal-3, VASH-1 and NGAL in GDM patients is increased especially the patients with early renal impairment. The prediction of triple combination for early renal impairment in GDM patients is more effective than that of patients with GDM alone.

Influencing factors and significance of plasma receptor interacting protein 3 level in preterm infants

ZHU Haijuan, YANG Zuming, FENG Zongtai, GAO Chuchu, CAI Yan, GU Danfeng

2026, 46(3):  427-430.  doi:10.16352/j.issn.1001-6325.2026.03.0427

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Objective To explore the clinical influencing factors and significance of plasma receptor interacting protein 3 (RIP3) level in preterm infants. Methods Plasma samples and clinical data of preterm infants admitted to the SuZhu Municipal Hospital from October 2019 and October 2021 were collected. Enzyme-linked immunoassay (ELISA) was used to detect plasma RIP3 level. Results A total of 92 preterm infants were included in the research project as infection group and non-infection group with 46 in each. Plasma samples were collected, including 46 from non-infection preterm infants, 46 from preterm infants at the onset of sepsis (before-treatment), and 32 from preterm infants 3 days after sepsis treatment (after-treatment). Comparing plasma RIP3 in different groups, it was found that the level of RIP3 in Post-treatment group (13.31±2.94)ng/mL and non-infection group (12.85±4.98)ng/mL were significantly lower than that in pre-treatment group(19.86±6.47)ng/mL (both P＜0.001), while there was no difference between after-treatment and non-infection.Multiple linear regression analysis found that infection was the main clinical factor affecting the plasma RIP3 level(β=0.571,95% CI:4 360.817-10 943.690,t=4.623,P＜0.01). The receiver operating characteristic(ROC) curve suggested that when the plasma RIP3 level reaches 15.16 ng/mL as a cut-off value, it has good predictive performance for sepsis [sensitivity=78.26%, specificity=73.91%, area under curve(AUC)=0.81]. Conclusions Plasma RIP3 level is closely related to infection in preterm infants and supports early diagnosis as well as treatment evaluation of sepsis.

Mini Reviews

Research progress in BK polyomavirus nephropathy

YANG Dan, YANG Feng

2026, 46(3):  431-434.  doi:10.16352/j.issn.1001-6325.2026.03.0431

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BK polyomavirus (BKPyV) typically enters host cells through caveolin-mediated endocytosis or clathrin-independent vesicle encapsulation, maintaining clinical latency without symptomatic manifestations. In immunocompromised hosts, particularly renal transplant recipients, viral reactivation within urothelial cells induces viruria, observed in 30%-40% of affected individuals. Subsequent retrograde viral migration along the urinary epithelium enables colonization of renal medullary tubules, establishing early-stage BKPyV nephropathy (BKPyVN). Progressive viral dissemination to cortical proximal tubules enhances replication kinetics, triggering cellular lyses and subsequent viremia in 10%-20% of cases. Persistent viral-induced cytopathology initiates cyclical epithelial damage and regenerative processes, ultimately manifesting as tubular atrophy, mononuclear inflammatory infiltration, and progressive interstitial fibrosis. This pathogenic cascade frequently culminates in irreversible allograft dysfunction and eventual graft failure.

Research progress in the treatment of NLRP3 inflammasome-mediated pyroptosis in cerebral ischemia-reperfusion injury

YANG Yiwei, SUN Xiaowei

2026, 46(3):  435-439.  doi:10.16352/j.issn.1001-6325.2026.03.0435

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Cerebral ischemia-reperfusion injury (CI/RI) is an important cause of neurological deterioration after ischemic stroke, and its mechanism is related to pyroptosis mediated by NLRP3 inflammasomes. The NLRP3 inflammasome is activated under the influence of multiple pathological mechanisms, promoting caspase-1-dependent gasdermin D lyses, triggering the formation of cell membrane pores and the release of inflammatory factors (IL-1β, IL-18), thereby leading to the occurrence of pyroptosis. Pyroptosis, as a type of cell death with obvious inflammatory response characteristics, It will cause and exacerbate neuroinflammatory responses.

Progress of ferroptosis in ventricular remodeling after acute myocardial infarction

Gulihuma·ABUDUKERANMU, Dilidaer·XILIFU, Adila·AZHATI

2026, 46(3):  440-444.  doi:10.16352/j.issn.1001-6325.2026.03.0440

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Ferroptosis is a new type of iron-dependent cell death, and its role in ventricular remodeling after acute myocardial infarction has attracted much attention in recent years. Studies have found that myocardial ischemia,hypoxia, iron overload and oxidative stress after AMI can activate the ferroptosis pathway, leading to cardiomyocyte death and interstitial fibrosis through mechanisms such as glutathione peroxidase 4 (GPX4) inactivation and lipid reactive oxygen species (ROS) accumulation, thereby promoting ventricular remodeling. Researches with animal models have confirmed that ferroptosis inhibitors or iron chelators can reduce myocardial injury and improve ventricular remodeling. In summary, inhibition of ferroptosis is expected to become a new strategy for the prevention and treatment of ventricular remodeling after AMI in the future.

Regulatory role of isthmin-1 in glucose and lipid metabolism and its clinical implications

HE Ping, WANG Yan

2026, 46(3):  445-449.  doi:10.16352/j.issn.1001-6325.2026.03.0445

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Isthmin-1 (ISM1), a novel adipokine, regulates glucose and lipid metabolism with a tissue-specific manner. In skeletal muscle and adipose tissue, ISM1 activates the insulin-independent mTORC2/PI3K/AKT signaling pathway, promoting GLUT4 translocation to the membrane, enhancing glucose uptake, and improving insulin sensitivity. In the liver, ISM1 suppresses the transcriptional activity of sterol regulatory element binding protein-1(Srebp1c) and the expression of downstream lipid synthesis genes, thereby reducing de novo lipogenesis. However, ISM1 exhibits pro-inflammatory potential in the adipose microenvironment, which may contribute to local inflammation and fibrosis. These tissue-specific regulatory effects highlight ISM1′s potential as a novel target for developing individualized, precision therapies for metabolic diseases.

Role of macrophage extracellular traps in infectious diseases

YUAN Jiamin, FANG Chengchao, JIANG Junsheng

2026, 46(3):  450-455.  doi:10.16352/j.issn.1001-6325.2026.03.0450

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Macrophage extracellular traps (METs) are newly discovered mechanism of immune system. Like neutrophil extracellular traps (NETs), their role in infectious diseases has not been fully elucidated. METs participate in host defense by releasing components such as DNA, histones, and antimicrobial proteins; However, their excessive or abnormal activation may exacerbate inflammatory responses and cause tissue damage. This article reviews the biological characteristics of METs, their activation pathways, and their potential mechanism of action in infectious diseases of various systems. It also explores METs- targeted therapeutic strategies, such as inhibiting METs formation or promoting their clearance to alleviate inflammatory responses, aiming to provide new theoretical basis and potential therapeutic targets for the treatment of infectious diseases.

Role of ferroptosis in vascular calcification diseases

WU Huilin, YUAN Fang

2026, 46(3):  456-461.  doi:10.16352/j.issn.1001-6325.2026.03.0456

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Ferroptosis, as an iron-dependent form of cell death, plays a crucial role in the onset and progression of vascular calcification (VC). Its core mechanisms involve intracellular iron overload, accumulation of lipid per oxidation, and the failure of antioxidant systems represented by GPX4/GSH. In the context of chronic kidney disease, diabetes, and atherosclerosis, processes of ferroptosis, such as the inhibition of the SLC7A11-GPX4 pathway, lipid metabolism disorders, and ferritinophagy, promote the osteoblast-like trans-differentiation of vascular smooth muscle cells (VSMCs); enhance oxidative stress and inflammatory responses, thereby accelerating calcium and phosphate deposition and vascular calcification. Targeting ferroptosis pathways significantly reduces calcification in experimental models, suggesting potential therapeutic strategies for VC.

Medical Education

A survey on the effectiveness of residency standardized training in periodontology

ZHANG Xin, ZHANG Xinyuan, DONG Xue, ZHOU Lian, DONG Haitao, GUO Chunlan

2026, 46(3):  462-466.  doi:10.16352/j.issn.1001-6325.2026.03.0462

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Objective To investigate the current status and competency of residency training graduates on periodontal diagnosis and treatment at Department of Stomatology, in Peking Union Medical College Hospital(PUMCH) and to evaluate the training outcomes of standardized periodontal training in order to support optimizing the training curriculum. Methods The questionnaires were distributed to trainees who had completed standardized training in the Department of Stomatology at PUMCH. The survey covered their current clinical practice in receiving periodontal patients, diagnostic and treatment capabilities, application of periodontal-related technologies during training, main problems encountered in clinical work, and evaluation of the training program. Results A total of 46 valid questionnaires were collected in this survey. Of the respondents, 84.78% treated patients with periodontal complaints with routine method, 89.13% performed sub-gingival scaling and root planning. In the view point of clinical practice, poor patient compliance (82.61%) and complex systemic disease management (69.57%) were identified as the primary challenges. Training needs were primarily concentrated in three areas: basic periodontal surgery(86.96%), relationship between systemic diseases and periodontitis (56.52%), patient communication and compliance management (39.13%). Overall, 65.22% of trainees considered the complexity of cases encountered during standardized training to be well-matched with actual clinical practice, and the average rating for the helpfulness of periodontal training was 4.5 out of 5. Conclusions The standardized periodontal training has achieved remarkable results. Future training should focus on strengthening content related to systemic disease management, doctor-patient communication skills and periodontal surgery.