Loading...

Table of Content

    05 August 2024, Volume 44 Issue 8
    Special Issues:Pulmonary Hypertension
    Anti-coagulation therapy for pulmonary hypertension: necessity and dilemmas
    HU Song, HUA Lu, ZHANG Jian
    2024, 44(8):  1062-1067.  doi:10.16352/j.issn.1001-6325.2024.08.1062
    Asbtract ( 77 )   PDF (792KB) ( 28 )  
    References | Related Articles | Metrics
    Pulmonary hypertension (PH) is a rare and life-threatening disease. Over past two decades, rapid advancements in treatment techniques have significantly improved the prognosis of two major subgroups of PH entities: pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH). Given the underlying pathological feature of in situ thrombosis of small arteries, anti-coagulation was previously considered to be a supportive therapy for PAH to improve prognosis. However, due to a lack of robust evidence, it is not recommended by the current guidelines. In contrast, lifelong anticoagulation is recommended for CTEPH patients to prevent thrombus recurrence and in situ thrombosis, based on the thromboembolic etiology. Furthermore, with the advent of direct oral anticoagulants, there are now more options for anti-coagulation therapy in PH. Nevertheless, due to the complexity of PH etiology and the heterogeneity of treatment approaches, anti-coagulation management remains challenging. This article reviews and evaluates the current status and safety issue of anti-coagulation therapy for PH patients, providing guidance and insights for clinical practice and research in this field.
    Portopulmonary hypertension: advances and challenges in diagnosis and clinical treatment
    FU Zhigang, QIN Jia, TAN Jiangshan
    2024, 44(8):  1068-1073.  doi:10.16352/j.issn.1001-6325.2024.08.1068
    Asbtract ( 86 )   PDF (784KB) ( 24 )  
    References | Related Articles | Metrics
    Portopulmonary hypertension (PoPH) represents one of complications occurred in patients with portal hypertension, which is characterized by high mortality rate and poor prognosis. The pathogenesis of PoPH remains unclear; it is believed to involve a complex interplay of factors including hyperdynamic circulation, imbalance of vasoactive substances, genetic factors and inflammatory responses. Up to the present, there is no specific treatment or medication for PoPH. However, medications such as endothelin receptor antagonists, prostacyclins and their analogues, phosphodiesterase-5 inhibitors and guanylate cyclase stimulants have been applied in the treatment of PoPH patients. The efficacy and safety of these treatment approaches still require further validation through large-scale, multicentered and randomized controlled trials. Liver transplantation may benefit a sub-group of patients but need a comprehensive assessment of individual cases. This article reviews the diagnosis, epidemiology, pathophysiology and current therapeutic performance of PoPH to further understand the pathogenesis of the disease and to improve diagnosis and treatment. Future research should focus on the development of new therapeutic drugs and evaluation of long-term effects of existing treatment methods, thereby providing more effective and safer treatment options to patients with PoPH.
    Metabolomics of pulmonary hypertension: from pathological mechanisms to therapeutic targets
    DENG Yuanrui, WANG Xiaojian
    2024, 44(8):  1074-1079.  doi:10.16352/j.issn.1001-6325.2024.08.1074
    Asbtract ( 67 )   PDF (779KB) ( 111 )  
    References | Related Articles | Metrics
    Pulmonary hypertension (PH) is a severe cardiovascular disease characterized primarily by pulmonary vascular remodeling. Patients with PH typically exhibit significant metabolic abnormalities including disruptions in energy metabolism, alterations in lipid and amino acids metabolism. These metabolic disturbances are closely linked to pathophysiological processes such as pulmonary vascular remodeling, endothelial dysfunction and right ventricular hypertrophy. In recent years, there has been rapid progress in the field of metabolomics related to PH. From the early identification of differential metabolic products to the current exploration of potential therapeutic targets, metabolomics has deepened the understanding of the pathogenesis of PH. These researches have accelerated the discovery and screening of potential therapeutic targets, with some findings already translated into clinical practice to support diagnosis, treatment and prognostic evaluation of PH.
    Inflammatory cells and vascular remodeling in pulmonary arterial hypertension
    QIAN Xifeng, HUA Lu
    2024, 44(8):  1080-1087.  doi:10.16352/j.issn.1001-6325.2024.08.1080
    Asbtract ( 75 )   PDF (832KB) ( 24 )  
    References | Related Articles | Metrics
    Pulmonary arterial hypertension (PAH) is a severe and progressive pulmonary vascular disease mainly characterized by a continuous increase in pulmonary vascular resistance and rise of pulmonary artery pressure caused by pulmonary arteriolar lesions, ultimately resulting in right heart failure and even death. Pulmonary vascular remodeling is a characteristic pathological change of PAH, and its mechanism involves gene susceptibility, imbalance of vasoactive substances, abnormal energy metabolism and other potential factors. Recent studies have found that inflammatory reaction plays a crucial role in the mechanism of pulmonary vascular remodeling. Inflammatory cells are found to infiltrate and accumulate around the pulmonary vessels of PAH patients and of animal models. In addition, significantly high level of cytokines and auto-antibodies were also found in peripheral blood, which is closely related to poor prognosis of PAH. This article reviews the research progress about the potential role of inflammatory cells in the vascular remodeling of PAH and provides new ideas for developing of safe and effective treatment methods for PAH.
    Development of novel therapies targeting at dysregulated signaling pathways in pulmonary arterial hypertension
    GAO Yidan, JIANG Xuehan, ZHANG Hong, YANG Peiran
    2024, 44(8):  1088-1093.  doi:10.16352/j.issn.1001-6325.2024.08.1088
    Asbtract ( 59 )   PDF (1099KB) ( 26 )  
    References | Related Articles | Metrics
    Pulmonary arterial hypertension (PAH) is a complex pulmonary vascular disease characterized by progressive elevation of mean pulmonary artery pressure resulted from the pathological feature of pulmonary vascular remodeling. Without medical intervention, PAH can eventually lead to right heart failure and death of patients. Up to the present, there are few treatment options for PAH are still mainly function through pulmonary vasodilation. Although these treatments can alleviate symptoms, the prognosis remains poor. In recent years, breakthroughs have been made in understanding the pathogenesis of PAH, thus support the development of new treatment strategies targeting at dysregulation of signaling pathways in PAH. This review focuses on five critical pathways and the relevant drugs those entered phase Ⅱ clinical trials and discusses their therapeutic potential, so to provide a basis for future research on targeting therapies for PAH patients.
    Original Articles
    Nervous protection provided by notoginsenoside Rg1 in rat model with Alzheimer′s disease
    WANG Tingting, WEI Huan, YANG Yongli, ZHOU Xian, HU Yang
    2024, 44(8):  1094-1100.  doi:10.16352/j.issn.1001-6325.2024.08.1094
    Asbtract ( 76 )   PDF (1828KB) ( 53 )  
    References | Related Articles | Metrics
    Objective To explore the mechanism of notoginsenoside Rg1 in preventing and treating Alzheimer′s disease (AD). Methods Rat model of AD was established by injecting amyloid beta peptide 1-42(Aβ1-42) into the lateral ventricle of SD rats. Then the animals were randomly divided into three groups: sham-operated group, model group and Rg1 treatment group. The treatment group was treated with Rg1 gavage and the sham-operated group was treated with saline gavage. Learning and memory capacity of rats were examined by Morris water maze experiment (MWM). Moreover, the contents of MDA and SOD in cerebral cortex were detected by chemical colorimetry; immuno-histochemistry was used to detect caspase-3 protein in the cerebral cortex and Western blot was employed to detect the expression of p38 and p-p38 proteins. Results Compared with the sham-operated group, the model group had a prolonged escape latency, reduced stay time in the target quadrant and reduced frequency of leaping over platform; increased MDA and decreased SOD in cerebral cortex; increased caspase-3 protein-positive neurons. The difference of p38 expression was not statistically significant and the phosphorylation of p38 was upregulated(P<0.05). The rats in Rg1 treatment group had a shorter escape latency, increased stay time in quadrant Ⅲ, increased frequency of leaping over platform, decreased caspase-3 positive neurons and the phosphorylation level of p38,decreased MDA and increased SOD compared with the model group(P<0.05). Conclusions Rg1 significantly improves learning and memory capacities, increases antioxidant capacity and plays neuro-protective effect in AD rat model by inhibition of p38 activation.
    Inhibition of sigma-1 receptor reduces DRG cell apoptosis of rats with neuropathic pain
    YU Dongling, MO Shaoe, FU Wen, CHEN Shi, XIE Chouqin, LAN Yuyan
    2024, 44(8):  1101-1106.  doi:10.16352/j.issn.1001-6325.2024.08.1101
    Asbtract ( 78 )   PDF (4817KB) ( 25 )  
    References | Related Articles | Metrics
    Objective To investigate the effect of sigma-1 receptor (sig-1R) inhibition on apoptosis in the dorsal root ganglion (DRG) of rats with sciatic nerve chronic constriction injury (CCI)-mediated neuropathic pain. Methods Rats undergoing intrathecal intubation were randomly divided into three groups with 12 in each: sham group, model group (CCI modeling one week after intrathecal intubation) and sig-1R inhibitor group (BD1047 group) that was injected intrathecally on the fourth, fifth, and sixth days after the CCI operation. The mechanical withdrawal threshold (MWT) of rats was detected on the day before surgery and then first, third, fifth and seventh days after surgery. The expression of sig-1R, Bcl-2 and Bax was detected by Western blot and immunofluorescence in DRG cell; TUNEL staining microscopy was used to observe the apoptosis of DRG cells. The changes of endoplasmic reticulum and mitochondria were observed by transmission electron microscopy of DRG cells. Results Compared with the sham group, the model group showed a decreased MWT at all time points after surgery, up-regulation of DRG cell apoptosis, up-regulation of sig-1R and Bax, down-regulation of Bcl-2, swelling of endoplasmic reticulum, disruption of mitochondrial membrane and reduction of mitochondrial cristae in the DRG cell endoplasmic reticulum after surgery(P<0.05).BD1047 group showed elevated MWT at the fifth and seventh postoperative days, down-regulation of DRG cell apoptosis, down-regulated expression of sig-1R and Box, up-regulated expression of Bcl-2 and slightly damaged endoplasmic reticulum as well as mitochondria of DRG cells compared with model group(P<0.05). Conclusions Inhibition of sig-1R up-regulates mechanical withdrawal threshold and reduces DRG cell apoptosis in CCI rats.
    Docosahexaenoic acid inhibits proliferation of human colon cancer cell line HT-29
    YAO Anjun, CHEN Lingzi, JIN Huixian
    2024, 44(8):  1107-1112.  doi:10.16352/j.issn.1001-6325.2024.08.1107
    Asbtract ( 61 )   PDF (2184KB) ( 26 )  
    References | Related Articles | Metrics
    Objective To investigate the effect of docosahexaenoic acid (DHA) on human colon cancer cell line HT-29 and underlying mechanism. Methods Human colon cancer cell line HT-29 was incubated with DMSO (control), DHA (25, 50, 100 μmol/L) and 100 μmol/L DHA and/or 30 μmol/L 740Y-P. Proliferation was examined by MTT; apoptosis was detected by annexin V-FITC/PI. Western blot was used for detection of protein expression of Bcl-2, Bax apoptosis-related protein and PI3K/Akt/mTOR pathway, and RT-qPCR was used for checking mRNA expression of NLRP3/Caspase-1/IL-1β pathway. Results Compared with the control group, DHA 25, 50,and 100 μmol/L treatment of HT-29 cells resulted in decreased cell survival (P<0.05), increased apoptosis(P<0.05), decreased Bcl-2/Bax ratio(P<0.05) and decreased phosphorylation of PI3K, Akt and mTOR in HT-29 cells(P<0.05 or P<0.01). Expressions of NLRP3, Caspase-1 and IL-1β mRNA were decreased (P<0.05). In addition, cell viability, protein phosphorylation (p-PI3K, p-Akt, p-mTOR)and relative mRNA expression of NLRP3, Caspase 1, and IL-1β were lower in HT-29 cells which were co-incubated with DHA 100 μmol/L and 740Y-P 30 μmol/L than those in the control group (P<0.05 or P<0.01) and 740Y-P 30 μmol/L group (P<0.05), while higher than that of DHA 100 μmol/L group(P<0.05 or P<0.01). Conclusions DHA inhibits the proliferation of human colon cancer cell line HT-29, its mechanism is potentially related to the inhibition of PI3K/Akt/mTOR and NLRP3/Caspase-1/IL-1β signaling pathways.
    Knockdown of lncRNA UCA1 reduces gemcitabine resistance of human bladder cancer cell line T24
    ZHOU Changdong, LIN Yang, SUN Kai, TIAN Yuxin
    2024, 44(8):  1113-1119.  doi:10.16352/j.issn.1001-6325.2024.08.1113
    Asbtract ( 66 )   PDF (3592KB) ( 24 )  
    References | Related Articles | Metrics
    Objective To investigate the in vitro effect of lncRNA UCA1 on gemcitabine (GEM) resistance of bladder cancer cell line T24 and its related molecular mechanism. Methods The mRNA expression of UCA1 in T24 cells and in T24/GEM cells was detected by RT-qPCR. The T24/GEM cells were incubated with varying concentrations (0.1, 1, and 10 μmol/L) of GEM for 48 hrs. LC3 staining microscopy was employed to visualize autophagic puncta, while the expression of autophagy-related proteins was assessed by Western blot. UCA1-shRNA and UCA1-shRNA+ pcDNA-Bcl-2 were transferred into T24/GEM cells, the sensitivity of cells to GEM was evaluated by MTT method and flow cytometry; the expressions of p53 and Bcl-2 were detected by Western blot. Results The expression level of UCA1 in T24/GEM cells was significantly higher than that of parental T24 cells (P<0.05). The concentration of GEM in the range of 0-10 μmol/L significantly induced dose-dependent autophagy in T24/GEM cells (P<0.05). Knockdown of UCA1 enhanced the sensitivity of T24/GEM cells to GEM (P<0.05), while reducing autophagy (P<0.05) and down-regulating the expression of p53 and Bcl-2(P<0.05). Over-expression of Bcl-2 partially reversed the GEM sensitization and autophagy inhibition of UCA1-shRNA in T24/GEM cells (P<0.05). Conclusions Knockdown of lncRNA UCA1 reduces GEM resistance of T24/GEM cells by inhibiting Bcl-2 mediated autophagy.
    Association of T helper cells and cytokines with abdominal obesity in Hashimoto′s thyroiditis
    Jazyra ZYNAT, LI Suli, ZHANG Kaidi, MA Fuhui, MA Guoying, GUO Yanying
    2024, 44(8):  1120-1125.  doi:10.16352/j.issn.1001-6325.2024.08.1120
    Asbtract ( 51 )   PDF (792KB) ( 16 )  
    References | Related Articles | Metrics
    Objective To investigate the correlation between abdominal obesity and autoimmune thyroid disease in the view point of helper T cells and cytokines. Methods Clinical and laboratory data were collected from 108 patients with Hashimoto′s thyroiditis (HT) plus abdominal obesity and 122 patients of Hashimoto′s thyroiditis without abdominal obesity who visited the People′s Hospital of Xinjiang Uygur Autonomous Region and also from the control population. Abdominal circumference was measured, and patients in the HT patients were grouped according to whether they were abdominally obese or not. The thyroglobulin antibody (TgAb) and thyroid peroxidase antibody (TPOAb) were detected, and the ratio of helper T cells and related cytokines were detected by flow cytometry and enzyme-linked immunosorbent assay. Results The abdominal circumference of the TgAb-positive group was higher than that of the TgAb-negative group (P<0.05). Correlation analysis suggested that abdominal circumference was significantly and positively correlated with TgAb and IL-4 but negatively correlated with Th1. After correcting for gender and age, and abdominal obesity and IL-4 were risk factors for TgAb antibody positivity OR=3.080(95% CI:1.022-9.284) and OR=1.296(95% CI:1.022-9.284), both with P<0.05. Conclusions Abdominal obesity may be an influential factor in TgAb antibody positivity, with larger abdominal circumference having higher TgAb antibody titers, lower Th1 levels, and higher IL-4 levels. Visceral adiposity may exacerbate autoimmune damage of thyroid tissue by disruption of helper T cell pathway.
    Effect of artesunate on neuroinflammation in depressed mouse model by regulating cGAS-STING signaling pathway
    GAO Chao, ZHANG Runhan, WANG Wei, ZHAO Manting, JIAO Yan, LI Zhe
    2024, 44(8):  1126-1132.  doi:10.16352/j.issn.1001-6325.2024.08.1126
    Asbtract ( 80 )   PDF (2802KB) ( 52 )  
    References | Related Articles | Metrics
    Objective To investigate the effect of artesunate (ART) on neuroinflammation in depressed mice by regulating the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon gene (STING) pathway. Methods Mice were divided into model group, control group, low-dose ART group, high-dose ART group, fluoxetine group, and high-dose ART+RocA (cGAS-STING pathway activator) group. Sugar solution consumption experiment and forced swimming experiment were applied to evaluate the depressive behavior of mice; HE staining microscopy was applied to detect pathological changes in hippocampal tissue; ELISA method was applied to detect the level of interleukin-6(IL-6), tumor necrosis factor-α(TNF-α), serotonin(5-HT) and dopamine (DA); TUNEL staining microscopy was applied to detect neuronal apoptosis; Western blot was applied to detect Bcl-2 associated X protein (Bax), p53, cGAS, and STING proteins. Results Compared to the control group, the mice in the model group exhibited neuronal pustule degeneration, the sugar water consumption rate, level of 5-HT and DA decreased, the rest time of forced swimming increased. The level of IL-6 and TNF-α, neuronal apoptosis rate, expression of Bax, p53, cGAS, and STING proteins all elevated (P<0.05); Compared with model group, the damage to hippocampus neurons in the ART low-dose group, ART high-dose group and fluoxetine group neuronal pustular degeneration was alleviated, while sugar water consumption rate, 5-HT, and DA levels increased, the rest time of forced swimming reduced, the level of IL-6 and TNF-α, neuronal apoptosis rate and the expression of Bax, p53, cGAS, and STING proteins reduced (P<0.05); RocA reversed the improvement effect of high-dose ART on depression in mice. Conclusions ART inhibits neuroinflammation and neuronal apoptosis in depressed mice, and up-regulates amine neurotransmitters expression. The mechanism is potentially related to the blocking of cGAS-STING pathway.
    Factors contributing to the occurrence of thyroid nodules and the correlation between adult Hcy, AGR and thyroid autoantibodies
    LI Xiufen, SUN Taran, FENG Yunxia, NIU Lili, XIE Xiaoxie, AN Yang, LI Xin
    2024, 44(8):  1133-1136.  doi:10.16352/j.issn.1001-6325.2024.08.1133
    Asbtract ( 59 )   PDF (749KB) ( 27 )  
    References | Related Articles | Metrics
    Objective To investigate the factors involved in the development of thyroid nodules and the correlation between homocysteine (Hcy) and albumin-globulin ratio (AGR) and thyroid autoantibodies in adults. Methods As a retrospective study, a total of 1 427 people who received physical examination at the Second Hospital Affiliated to Hebei North College from October 2019 to August 2020 and the clinical data of the subjects who fulfilled the criteria of NAR were selected for analysis by simple random sampling. All of subjects underwent thyroid color ultrasound scanning and were divided into a control group (without thyroid nodules, n=52) and an observation group (with thyroid nodules, n=48). The general clinical data of the two study groups were compared, and the correlation between Hcy and AGR and thyroid autoantibodies was analyzed.Confunding factors affecting the incidence of thyroid nodules were screened using multifactorial unconditional logistic regression analysis. Results The observation group showed statistically significant differences in gender, age, diastolic blood pressure, systolic blood pressure, Hcy, AGR, TGAb, and TPOAb as compared to the control group (P<0.05); Using adult Hcy as the dependent variable and Spearman′s correlation analysis of AGR, TGAb and TPOAb, adult Hcy was negatively correlated with AGR (r=-0.384, P<0.05) and TGAb and TPOAb were positively correlated (r=0.218, 0.224, P<0.05); Using age, sex, diastolic blood pressure, systolic blood pressure, Hcy, AGR TGAb and TPOAb as independent variables and thyroid nodules as dependent variables, a multifactor logistic regression analysis was performed in 100 subjects who experienced physical check. The analysis showed that age ≥40 years and female were relevant factors for the development of thyroid nodules factors (P<0.05), Hcy, AGR, TGAb and TPOAb were correlated with thyroid nodules (P<0.05). Conclusions Thyroid nodules are more common in middle-aged women, and there is a correlation between Hcy, AGR, TGAb, and TPOAb levels and thyroid nodules. Regular thyroid screening examination should be carried out based on the above indicators.
    Whole blood NPM1, MCP-1 and intestinal flora are associated with gastric cancer progression and prognosis
    HOU Nan, LIU Yuan, GAO Jun, WANG Jing, YUAN Meng
    2024, 44(8):  1137-1142.  doi:10.16352/j.issn.1001-6325.2024.08.1137
    Asbtract ( 62 )   PDF (908KB) ( 18 )  
    References | Related Articles | Metrics
    Objective To investigate the association of whole blood nucleophosmin 1(NPM1), monocyte chemotactic protein-1 (MCP-1), and intestinal flora with gastric cancer progression and prognosis. Methods A total of 120 patients with gastric cancer who were admitted to the Nanyang Second People′s Hospital from May 2018 to May 2020 were selected as the gastric cancer group, 120 patients with benign gastric lesions underwent gastroscopy in the same period were selected as the benign gastric lesions group, and 120 patients with healthy physical examinations in the same period were selected as the control group. RT-qPCR was used to detect mRNA expression of NPM1 and MCP-1. The intestinal microbiota was examined by MicroScan microbial identification analysis system; The correlation between NPM1, MCP-1 and intestinal microbiota was analyzed by Pearson method. Multivariate COX regression was used to analyze the influencing factors of prognosis in gastric cancer patients. Results The level of NPM1 mRNA,exuberance of Bifidobacterium and Lactobacillus in the control group, gastric benign lesion group, and gastric cancer group decreased sequentially (P<0.05), whereas MCP-1 mRNA, Enterococcus, and Escherichia coli increased sequentially (P<0.05). Serum NPM1 mRNA, Bifidobacterium and Lactobacillus in stage Ⅲ-Ⅳ of gastric cancer were obviously lower than those found in stage Ⅰ-Ⅱ(P<0.05), while MCP-1 mRNA, Enterococcus and Escherichia coli were obviously more than those found in stage Ⅰ-Ⅱ(P<0.05). Pearson correlation analysis showed that, there was a negative correlation between serum NPM1 mRNA and MCP-1 mRNA levels in gastric cancer patients (P<0.05), NPM1 mRNA was positively correlated with Bifidobacterium and Lactobacillus(P<0.05) and negatively correlated with Enterococcus and Escherichia coli(P<0.05). MCP-1 mRNA was negatively correlated with the quantity of Bifidobacterium and Lactobacillus(P<0.05) but positively correlated with Enterococcus and Escherichia coli(P<0.05). The level of NPM1 mRNA, quantity of Bifidobacterium and Lactobacillus in the poor prognosis group were obviously lower than those found in the good prognosis group (P<0.05), while the level of MCP-1 mRNA, quantity of Enterococcus and Escherichia coli were obviously higher than those in the good prognosis group (P<0.05). COX regression analyses showed that MCP-1 mRNA, Enterococcus and Escherichia coli were risk factors affecting the prognosis of gastric cancer patients (P<0.05), while NPM1 mRNA, Bifidobacterium, and Lactobacillus were protective factors (P<0.05). Conclusions Decreased level of NPM1, decreased counting of Bifidobacterium intestinalis and Lactobacillus, increased level of MCP-1, increased counting of Enterococcus and Escherichia coli are strongly associated with gastric cancer progression and poor prognosis.
    Atractylodes macrocephala lactone Ⅲ alleviates nerve function injury in rat model with cerebral infarction
    ZHANG Qiuping, YANG Yuejun, ZHANG Caili
    2024, 44(8):  1143-1148.  doi:10.16352/j.issn.1001-6325.2024.08.1143
    Asbtract ( 54 )   PDF (3496KB) ( 10 )  
    References | Related Articles | Metrics
    Objective To explore the effect of atractylodes macrocephala lactone Ⅲ (AML Ⅲ)on nerve injury of rats with cerebral infarction. Methods The rats were randomly divided into sham operation group, model group (modified Longa thrombus method to prepare rat cerebral infarction model), low and high dose of AML Ⅲ group (AMLⅢ-L,AMLⅢ-H) and high dose AML Ⅲ +EX527 (SIRT1 inhibitor) group (AMLⅢ-H-EX527). Neurological function was assessed by Zea-Longa score. Serum tumor necrosis factor (TNF-α) and interleukin (IL-6, IL-1β) were measured by ELISA; The level of super oxide dismutase activity (SOD), malonaldehyde content (MDA), and catalase activity (CAT) in brain tissue was detected by commercially available kit; pathological changes of hippocampus tissue and the area of cerebral infarction were observed by HE staining and TTC staining microscopy respectively. Apoptosis of brain cells was identified by TUNEL staining; protein expression of Bax, Bcl-2, SIRT1, and Nrf2 in rat brain tissue was detected by Western blot assay. Results After the intervention by AML Ⅲ, the pathological injury of hippocampus neurons in rats was alleviated. The neurological function score, serum TNF-α, IL-6 and IL-1β levels, apoptosis rate, cerebral infarction size,MDA level and Bax protein expression were all decreased. SOD and CAT activity, SIRT1, Nrf2, Bcl-2 and protein expression were all increased (P<0.05); EX527 was able to alleviate the protective effect of AML Ⅲ on neural function damage in rats with cerebral infarction. Conclusions Atractylodes macrocephala lactone Ⅲ reduces the nerve function injury in rat models with cerebral infarction.
    Bone marrow mesenchymal stem cell-derived exosome inhibits high glucose-induced EMT of peritoneal mesothelial cells
    ZHAO Junli, ZHU Junjun, ZHAN Qiunan, LIU Miao
    2024, 44(8):  1149-1156.  doi:10.16352/j.issn.1001-6325.2024.08.1149
    Asbtract ( 69 )   PDF (3595KB) ( 25 )  
    References | Related Articles | Metrics
    Objective To investigate the effects of bone marrow mesenchymal stem cell-derived exosomes (BMSCs-Exo) on the regulation of epithelia-mesenchymal transition (EMT) in human peritoneal mesothelial cells (HPMCs) treated with glucose-based peritoneal dialysis fluid (PDF). Methods BMSCs-Exo were verified by transmission electron microscopy(TEM), nanoparticle tracking analyzer(NTA) and Western blot. Cultured HPMCs(HMrSV5) were divided into 5 groups: control group, high glucose-based PDF (1.5%, 2.5%, and 4.25%) group, siNLRP3 group, siNC group and BMSCs-Exo treated group. Expression of E-cadherin, vimentin, α-smooth muscle actin (α-SMA) and NLRP3 inflammasome-related proteins were detected by Western blot. Real time RT-PCR was used to detected the expression of α-SMA, E-cadherin and TGF-β1 mRNAs in HMrSV5 cells. The concentration of TGF-β1, IL-1β and IL-18 in the culture supernatant was determined by ELISA. Results The exosomes isolated were spherical and double-membrane vesicles with 40-150 nm in diameter, which expressed CD9, CD81, TSG101 and Alix protein. Our results showed that the level of α-SMA and vimentin were significantly up-regulated and E-cadherin (epithelial marker) was significantly decreased in HMrSV5 cells treated with high glucose PDF compared with the normal HMrSV5 cells. The expression of NLRP3,pro-caspase-1 and pro-IL-1β were also significantly up-regulated in HMrSV5 cells treated with high glucose PDF compared with the normal HMrSV5 cells. The level of TGF-β1, IL-1 β and IL-18 in high glucose PDF treated HMrSV5 cells culture supernatant was up-regulated in a dose dependent manner. The protein level of α-SMA was decreased and E-cadherin level was increased by an NLRP3 siRNA to inhibit the activation of NLRP3. Compared with 4.25% PDF treated cells, E-cadherin expression was up-regulated, while the expression of α-SMA and vimentin were down-regulated in BMSCs-Exo treatment cells (P<0.05). Furthermore, the protein expression of NLRP3, pro-caspase-1 and pro-IL-1β in 4.25% PDF-treated HMrSV5 cells were significantly reduced by BMSCs-Exo. BMSCs-Exo also reduced the level of TGF-β1, IL-1β and IL-8 in the 4.25% PDF-treated HMrSV5 cells culture supernatants (P<0.05). Conclusions High glucose PDF-induced EMT in HPMCs might be mediated by NLRP3 inflammatory signaling pathway, which can be inhibited by BMSCs-Exo.
    Clinical Sciences
    Analysis of clinical features of hypereosinophilic syndrome complicated with peripheral arterial embolism
    HAN Yingdong, WANG Song, ZHANG Yun, ZENG Xuejun
    2024, 44(8):  1157-1161.  doi:10.16352/j.issn.1001-6325.2024.08.1157
    Asbtract ( 68 )   PDF (888KB) ( 25 )  
    References | Related Articles | Metrics
    Objective To improve the understanding of hypereosinophilic syndrome (HES) complicated with peripheral arterial embolism through analyzing the clinical features and therapeutic effect. Methods Among 176 inpatients with peripheral arterial embolism in Peking Union Medical College Hospital from April 2012 to October 2021, 13 patients complicated with HES were involved according to the inclusion and exclusion criteria. All patients were diagnosed with peripheral arterial embolism by imaging examination. After gender and age matching, 39 HES patients who were hospitalized in the same period but without peripheral arterial embolism were selected as the control with the ratio of 1∶3. Clinical features, therapy response and prognosis were compared between the two groups. Results Eleven of the 13 patients were male. The main involved arteries included popliteal artery, dorsalis pedis artery, ulnar artery and radial artery. The proportion of peripheral nerve involvement in case group was significantly higher than in the control group (P<0.05); and the proportion of gastrointestinal involvement(P<0.05) and eosinophil level (P<0.05) were significantly lower than that of control group. There were 92.3%, 61.5% and 76.9% of the patients in case group received anticoagulant therapy, antiplatelet therapy and immunosuppressive therapy respectively, the percentages were significantly higher than that in control group(P<0.01). According to eosinophil counts before and after therapy, 84.6% and 56.5% of the patients in the case and control groups achieved complete remission and the partial remission rates were 15.4% and 25.6% respectively. Conclusions Patients with hypereosinophilia syndrome and peripheral arterial embolism commonly experience involvement of the peripheral nerves and skin. Vascular embolism is mainly caused by arterial embolization of the extremities. After treatment with hormones, immunosuppressants, anticoagulants and/or antiplatelet therapy, this group of patients has a good prognosis.
    Analysis of CT imaging features and causes of miss diagnosis of ectopic pancreas based on endoscopy
    WANG Yuqi, LUO Dinghao, CHAI Xiaoyuan, SUN Peng, MA Xiaoxuan
    2024, 44(8):  1162-1164.  doi:10.16352/j.issn.1001-6325.2024.08.1162
    Asbtract ( 55 )   PDF (1165KB) ( 10 )  
    References | Related Articles | Metrics
    Objective To explore the imaging manifestations of ectopic pancreas based on endoscopic findings in order to find out the causes of miss diagnosis and to improve the diagnostic accuracy. Methods The clinical and CT imaging data of ectopic pancreas patients who underwent CT examination and confirmed by endoscopy and pathology microscopy at Air Force Medical Center from July 2018 to March 2023 were collected. Their imaging characteristics were analyzed according to the endoscopic findings and the miss diagnosis was analyzed. Results There were 13 patients with ectopic pancreas and 3 of them had no obvious symptoms. Ten patients presented with gastrointestinal symptoms, including epigastric discomfort and pain, incomplete obstruction, and melena. Lesion sites: 8 cases were located in the gastric antrum and 5 cases were located in the small intestine. In this group, two patients showed apical erosions and glandular opening-like depressions on endoscopic results, but only one patient showed a “ductal sign” shown by CT scanning. None of the 13 patients in this group made ectopic pancreatic diagnosis on imaging, of which 4 were diagnosed as thickening of the gastrointestinal tract wall, 3 were diagnosed as gastrointestinal stromal tumor, 3 were diagnosed as benign tumors and 3 had no obvious abnormalities. Conclusions The imaging diagnosis of ectopic pancreas should be made by closely combinating with the results of endoscopy to improve the accuracy of imaging diagnosis. CT is of great significance for the diagnosis of ectopic pancreas, and adequate preparation before gastrointestinal examination is an important step to avoid misdiagnosis.
    Mini Reviews
    Progress on the role of MBD2 pathway in severe asthma
    WU Dingjiang, ZHANG Xiufeng
    2024, 44(8):  1165-1169.  doi:10.16352/j.issn.1001-6325.2024.08.1165
    Asbtract ( 57 )   PDF (759KB) ( 54 )  
    References | Related Articles | Metrics
    Severe asthma is a chronic inflammatory disease that is not sensitive to glucocorticoid treatment. In the pathogenesis of severe asthma, T helper cell 17(Th17) and interleukin 17 (IL-17) play an important role, mainly by aggregating the infiltration of neutrophil to aggravate the severity of asthma. Methyl-CpG-binding protein 2 (MBD2) plays an important role in the differentiation of Th17 cells from naive CD4+T cells,positively regulate Th17 differentiation and IL-17 expression. MBD2 binds to the CpG islands in the promoter region of interferon regulatory factor 4 (IRF4), suppressor of cytokine signaling 3 (SOCS3), hypoxia-inducible factor-1α (HIF-1α) and misshapen like kinase 1(MINK1), which leads to methylation, regulates the differentiation of Th17 cells, and participates in the pathogenesis of severe asthma.
    CD27/CD70 and idiopathic pulmonary fibrosis
    XU Yuncong, ZHENG Jinxu
    2024, 44(8):  1170-1174.  doi:10.16352/j.issn.1001-6325.2024.08.1170
    Asbtract ( 67 )   PDF (886KB) ( 54 )  
    References | Related Articles | Metrics
    Idiopathic pulmonary fibrosis (IPF) is a chronic interstitial lung disease marked by the significant involvement of fibroblasts, macrophages and lymphocytes. The CD27/CD70 axis is pivotal in shaping the immune microenvironment present in the fibrotic aeras of lungs. This mentioned interaction involves molecular pathways that work in tandem with lung immune cells, particularly exerting a suppressive influence in the early phases of pulmonary fibrosis. Consequently, the CD27/CD70 axis presents a promising new target for immunotherapy in IPF.
    Role of SphK/S1P in cardiovascular diseases
    TANG Lihong, CHEN Chunling
    2024, 44(8):  1175-1179.  doi:10.16352/j.issn.1001-6325.2024.08.1175
    Asbtract ( 58 )   PDF (754KB) ( 21 )  
    References | Related Articles | Metrics
    Sphingosine-1-phosphate (S1P) is a highly active membrane phospholipid metabolite with important physiological roles in the cardiovascular system. Sphingosine kinase (SphK) is a lipase that is important for maintaining stable S1P levels in vivo. S1P exerts different physiological effects in cardiovascular diseases by catalytically regulating the binding of S1P to G protein-coupled receptors (S1PR1-5) on the cell surface, thus exerting different physiological effects in cardiovascular diseases.For example, they are involved in regulating the development of diseases such as atherosclerosis, myocardial ischemia-reperfusion injury, myocardial infarction, heart failure and other diseases, maintaining the barrier function of vascular endothelial cells, protecting the endothelial glycocalyx layer, leukocyte adhesion, inflammatory reactions and other pathophysiologic processes.
    Research progress of astrocyte phagocytosis in Alzheimer′s disease
    QIN Xiaoli, ZHAO Linna, FU Rong, GUO Yuying, XU Shixin
    2024, 44(8):  1180-1184.  doi:10.16352/j.issn.1001-6325.2024.08.1180
    Asbtract ( 88 )   PDF (2612KB) ( 37 )  
    References | Related Articles | Metrics
    Astrocytes are heavily activated in Alzheimer′s disease, engulfing damaged synapses, Aβ proteins, Tau proteins, apoptotic cells and other substrates. However, these substrates are difficult to degrade, accumulate as the disease progresses, and impair the phagocytosis of astrocytes. During phagocytosis, astrocytes recognize different substrates through a variety of phagocytosis receptors and partially degrade the substrates through degrading enzymes and lysosomal pathways. The accumulation of Aβ and Tau proteins in astrocytes caused astrocyte immune and metabolic disorders, and Aβ toxicity changed after phagocytosis. In addition, astrocytes and microglia form a complementary pattern and cooperate to complete phagocytosis through interaction. Regulating the pathway of astrocyte phagocytosis and degradation is believed to be a potential novo therapeutic for clinical treatment of Alzheimer′s disease.
    Progress of hydrogen sulfide in delaying brain aging
    SUN Fengqi, LUO Xiaoting, LIU Hong, SONG Yunjia
    2024, 44(8):  1185-1188.  doi:10.16352/j.issn.1001-6325.2024.08.1185
    Asbtract ( 49 )   PDF (738KB) ( 28 )  
    References | Related Articles | Metrics
    Brain aging is closely related to cognitive decline, neurodegenerative diseases, and vascular dementia. Hydrogen sulfide (H2S) can delay brain aging by regulating protein homeostasis, anti-oxidative stress, inhibiting inflammation, reducing brain cell apoptosis and improving microcirculation.
    Research progress on the type 1 diabetes induced sarcopenia
    PENG Qingyi, XU Lingling
    2024, 44(8):  1189-1193.  doi:10.16352/j.issn.1001-6325.2024.08.1189
    Asbtract ( 77 )   PDF (757KB) ( 83 )  
    References | Related Articles | Metrics
    The prevalence of sarcopenia in type 1 diabetes is higher than that in type 2 diabetes and non-diabetes patients. Screening, diagnosis and intervention of sarcopenia in type 1 diabetes patients as early as possible is of great significance for improving the life quality of these patients. The occurrence of sarcopenia in type 1 diabetes mellitus may be closely related to the decline of skeletal muscle function caused by the decrease of insulin-like growth factor-1, activation of inflammatory factors, mitochondrial dysfunction, and accumulation of advanced glycation end-products. At present, the mechanism of the occurrence and development of sarcopenia induced by type 1 diabetes is not completely clear, and the relevant new drug treatment lacks data support. Further in-depth research may bring a new direction for the prevention and treatment of sarcopenia in type 1 diabetes patients.
    Medical Education
    Teaching evaluation of the traditional Chinese medicine course by medical students from the reform pilot class in clinical medicine at Peking Union Medical College
    YANG Dan, WU Qunli, LIANG Xiaochun, SUN Hua, ZHANG Mengren, HAO Weixin, LIU Yi
    2024, 44(8):  1194-1197.  doi:10.16352/j.issn.1001-6325.2024.08.1194
    Asbtract ( 73 )   PDF (844KB) ( 63 )  
    References | Related Articles | Metrics
    Objective To evaluate the teaching performance of the traditional Chinese medicine (TCM)course for the first three grades of the “4+4” reform pilot class in clinical medicine at Peking Union Medical College. Methods An anonymous survey was conducted using Questionnaire Star and the responses from TCM Teaching Questionnaire completed by students were statistically analyzed and summarized. Results Most students expressed interest in TCM and deemed it necessary to study TCM course. They believed that teachers well prepared for teaching performance and the teaching content was well-aligned with the textbooks, syllabus, and lecture slides. The teaching content was closely integrated with clinical practice, and students were satisfied with the teaching methods and approaches. Conclusions Teaching evaluations help teachers to summarize their teaching experiences and improve the teaching quality of the TCM course.
    Practice and reflection on courses with idedogical-political elements in neurophysiology and pharmacology
    YU Xiaoli, JI Chao
    2024, 44(8):  1198-1200.  doi:10.16352/j.issn.1001-6325.2024.08.1198
    Asbtract ( 93 )   PDF (713KB) ( 41 )  
    References | Related Articles | Metrics
    Political and value education of curriculum is necessary for universities to implement the fundamental task of cultivating morality and talents. Physiology and pharmacology are bridge courses connecting basic medicine and clinical medicine, and the nervous system is an important component of them. The exploration and practice of idedogical-political elements in the courses of nervous system physiology and pharmacology are of great significance in the curriculum of basic medical education and are essential for the cultivation of top-notch innovative talents. Our research group explored the integration of political and value education cases in the courses of neurophysiology and pharmacology, and conducted preliminary practice and summary thinking, providing reference for future research on political and value education in other courses.