松果菊苷调节mTOR/STAT3信号通路对冠心病大鼠心肌细胞凋亡和炎症损伤的影响  

Influences of echinacoside on myocardial cell apoptosis and inflammatory injury in rats with coronary heart disease by regulating mTOR/STAT3 signaling pathway

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作  者:苏强 谢家和[1] 黄鹤[1] 曾山[1] 钟一鸣[1] SU Qiang;XIE Jiahe;HUANG He;ZENG Shan;ZHONG Yiming(Department of Cardiovascular Medicine,the First Affiliated Hospital of Gannan Medical University,Key Laboratory of Prevention and Treatment of Cardiovascu-lar and Cerebrovascular Diseases of Ministry of Education,Ganzhou 341000,China)

机构地区:[1]赣南医学院第一附属医院心血管内科,赣南医学院心脑血管疾病防治教育部重点实验室,赣州341000

出  处:《中国免疫学杂志》2024年第12期2574-2579,共6页Chinese Journal of Immunology

基  金:国家自然科学基金(82060098);赣州市指导性科技计划项目(GZ2019ZSF038)。

摘  要:目的:探讨松果菊苷(ECH)对冠心病(CHD)大鼠心肌细胞凋亡、炎症损伤及雷帕霉素(mTOR)/信号传导与转录激活因子3(STAT3)信号通路的影响。方法:选择12只SD大鼠为对照组(NC组),成功构建48只CHD大鼠模型,随机分为模型(Model)组、ECH组(50mg/kg)、mTOR激活剂MHY1485组(10mg/kg)、ECH^(+)MHY1485组(50mg/kgECH^(+)10mg/kg MHY1485)。4周后,通过生物机能实验系统记录心电图;试剂盒检测心肌C反应蛋白(CRP)、IL-6水平;HE和TUNEL染色观察心肌病理学和细胞凋亡;qRT-PCR检测心肌Bcl-2、Bax mRNA表达;Western blot检测心肌mTOR/STAT3通路蛋白表达。结果:与NC组相比,Model组大鼠心肌有明显坏死、水肿和炎症细胞浸润,ST段偏移幅度、IL-6、CRP水平、心肌细胞凋亡率、Bax mRNA表达、mTOR和p-STAT3/STAT3蛋白水平显著升高(P<0.05),Bcl-2 mRNA表达显著下降(P<0.05);与Model组相比,ECH组大鼠心肌损伤减轻,ST段偏移幅度、IL-6、CRP水平、心肌细胞凋亡率、Bax mRNA表达、mTOR和p-STAT3/STAT3蛋白水平显著下降(P<0.05),Bcl-2 mRNA表达显著上升(P<0.05);而MHY1485组大鼠以上指标呈相反趋势;MHY1485消除了ECH对CHD大鼠的有利影响。结论:ECH可能通过下调mTOR/STAT3通路减轻CHD大鼠心肌炎症损伤和细胞凋亡。Objective:To investigate influences of echinacoside(ECH)on myocardial cell apoptosis,inflammatory injury and mammalian target of rapamycin(mTOR)/signal transducer and activator of transcription 3(STAT3)signaling pathway in rats with coronary heart disease(CHD).Methods:A total of 12 SD rats were taken as control group(NC group),48 CHD rat models were successfully constructed,and randomly divided into model(Model)group,ECH group(50 mg/kg),mTOR activator MHY1485 group(10 mg/kg),ECH^(+)MHY1485 group(50 mg/kg ECH^(+)10 mg/kg MHY1485).After 4 weeks,electrocardiogram was recorded through biological function experimental system.Kits were used to detect myocardial C-reactive protein(CRP)and IL-6 levels.Myocardial pathology and apoptosis were measured by HE and TUNEL staining.qRT-PCR was used to detect myocardial Bcl-2,Bax mRNA expressions.Western blot was used to detect myocardial mTOR/STAT3 pathway protein expression.Results:Compared with NC group,Model group rats had obvious necrosis,edema and inflammatory cell infiltration,ST segment deviation,IL-6,CRP levels,cardiomyocyte apoptosis rate,Bax mRNA expression,mTOR and p-STAT3/STAT3 protein levels were significantly increased(P<0.05),Bcl-2 mRNA expression was significantly decreased(P<0.05).Compared with Model group,myocardial injury in ECH group was alleviated,ST segment shift,IL-6,CRP levels,cardiomyocyte apoptosis rate,Bax mRNA expression,mTOR and p-STAT3/STAT3 protein levels were were significantly decreased(P<0.05),Bcl-2 mRNA expression was significantly increased(P<0.05).The above indexes of MHY1485 group rats showed opposite trend.MHY1485 eliminates beneficial effects of ECH on CHD rats.Conclusion:ECH may reduce myocardial inflammatory injury and apoptosis in CHD rats by down-regulating mTOR/STAT3 pathway.

关 键 词:松果菊苷 mTOR/STAT3通路 冠心病 炎症 细胞凋亡 

分 类 号:R541.4[医药卫生—心血管疾病]

 

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