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目的 探讨氯吡格雷通过下调表皮生长因子受体(EGFR)对脂肪肝患者的改善效果。方法 通过动物实验和临床实验,分析氯吡格雷对斑马鱼转基因脂肪肝模型中的脂质含量及EGFR表达的影响。从2022年1月至2024年8月九江学院附属医院收治的心脑血管疾病合并脂肪肝患者中选取60例作为研究对象,随机分为对照组和观察组,每组30例。对照组服用其他抗血小板药物,观察组服用氯吡格雷,比较两组血糖水平、血脂水平、肝功能及脂肪肝严重程度等临床指标。结果 氯吡格雷通过下调EGFR信号通路,减少了斑马鱼转基因脂肪肝模型中的脂质含量。治疗前,两组临床指标(包括空腹血糖、餐后血糖、甘油三酯、胆固醇、低密度脂蛋白、高密度脂蛋白、肝功能指标、脂肪肝严重程度)比较差异均无统计学意义(P>0.05);治疗后,两组临床指标均有所改善,差异均有统计学意义(P<0.05)。结论 氯吡格雷通过下调EGFR可有效改善心脑血管疾病合并脂肪肝患者的各项指标,具有显著的治疗效果,值得在临床中推广。
Abstract:Objective Exploring the improvement effect of clopidogrel on patients with fatty liver by downregulating epidermal growth factor receptor(EGFR). Methods Analyze the effect of clopidogrel on lipid content and EGFR expression in zebrafish transgenic fatty liver model through animal experiments and clinical trials. Sixty patients with cardiovascular and cerebrovascular diseases combined with fatty liver admitted to Jiujiang University Affiliated Hospital from January 2022 to August 2024 were selected as the research subjects and randomly divided into a control group and an observation group, with 30 patients in each group. The control group received other antiplatelet drugs, while the observation group received clopidogrel. The improvement effect of fatty liver in the two groups was compared, including clinical indicators such as blood glucose levels, blood lipid levels, liver function, and severity of fatty liver. Results Clopidogrel reduces lipid content in zebrafish transgenic fatty liver models by downregulating the EGFR signaling pathway. Before treatment, there was no statistically significant difference in clinical indicators between the two groups(including fasting blood glucose,postprandial blood glucose, triglycerides, cholesterol, low-density lipoprotein, high-density lipoprotein, liver function indicators, and severity of fatty liver)(P >0.05); After treatment, both groups showed improvement in clinical indicators, with statistically significant differences(P<0.05).Conclusion Clopidogrel can effectively improve various indicators in patients with cardiovascular and cerebrovascular diseases complicated with fatty liver by downregulating EGFR, and has significant therapeutic effects, which is worth promoting in clinical practice.
[1]YOUNOSSI Z M, KO ENIG A B, ABDELATIF D, et al.Global epidemiology of nonalcoholic fatty liver disease—metaanalytic assessment of prevalence, incidence, and outcomes[J]. Hepatology, 2016, 64(1):73—84.
[2]KATSIKI N , PEREZ-MARTINEZ P , ANAGNOSTIS P ,et al. Is nonalcoholic fatty liver disease indeed the hepatic manifestation of metabolic syndrome[J]. Current Vascular Pharmacology, 2018, 16(3):219—227.
[3]HALMOS T, SUBA I. Non-alcoholic fatty liver disease, as a component of the metabolic syndrome, and its causal correla tions with other extrahepatic diseases[J]. Orvosi Hetilap, 2017,158(52):2051.
[4]KUMAR R, PRIYADARSHI R N, ANAND U. Non-alcoholic fatty liver disease:growing burden, adverse outcomes and associations[J]. Journal of Clinical and Translational Hepatology, 2020, 8(1):76.
[5]ESTES C, RAZAVI H, LOOMBA R, et al. Modeling the epidemic of nonalcoholic fatty liver disease demonstrates an exponential increase in burden of disease[J]. Hepatology ,2018, 67(1):123—133.
[6]TAI T,SHAO Y Y, ZHENG Y Q, et al.“Clopidogrel ameliorates high-fat diet-induced hepatic steatosis in mice through activation of the AMPK signaling pathway and beyond”[J]. Frontiers in Pharmacology,2024,15(1):149—155.
[7]TOEDA Y, KASAMATSU A, KOIKE K, et al. FBLIM1 enhances oral cancer malignancy via modulation of the epidermal growth factor receptor pathway[J]. Mol Carcinog,2018,57(12):1690—1697.
[8]LUO J C, HUO T I, HOU M C, et al.Clopidogrel delays gastric ulcer healing in rats[J]. Eur J Pharmacol, 2012,695(1):112—119.
[9]LIANG D, CHEN H, ZHAO L, et al. Inhibition of EGFR attenuates fibrosis and stellate cell activation in diet-induced model of nonalcoholic fatty liver disease[J]. Biochim Biophys Acta Mol Basis Dis,2018,1864(1):133—142.
[10]BANO S, COPELAND M A, STOOPS J W, et al.Hepatocyte-specific epidermal growth factor receptor deletion promotes fibrosis but has no effect on steatosis in fast-food diet model of metabolic dysfunction-associated steatotic liver dis ease[J]. Cell Mol Gastroenterol Hepatol,2024,18(4):1013—1020.
[11]LEE K C, WU P S, LIN H C. Pathogenesis and treatment of non-alcoholic steatohepatitis and its fibrosis[J]. Clin Mol Hepatol,2023,29(1):77—98.
[12]DALBENI A, CASTELLI M, ZONCAPE M, et al. Platelets in Non-alcoholic Fatty Liver Disease[J].Front Pharmacol ,2022,13(1):26—36.
基本信息:
DOI:10.16096/J.cnki.nmgyxzz.2025.57.11.005
中图分类号:R575.5
引用信息:
[1]罗洋,李力,杜垚,等.氯吡格雷通过下调EGFR改善脂肪肝的机制及疗效研究[J].内蒙古医学杂志,2025,57(11):1308-1312.DOI:10.16096/J.cnki.nmgyxzz.2025.57.11.005.
基金信息:
江西省卫生健康委科技计划项目(编号:202212015)