双参通脉颗粒抑制ERK1/2-NF-κB信号通路改善急性心肌梗死模型大鼠心肌损伤作用机制研究  

Mechanism of Shuangshen Tongmai Granules Improving Myocardial Injury in Model Rats with Acute Myocardial Infarction by Inhibiting ERK1/2-NF-κB Signaling Pathway

作　　者：吴杨[1] 王秀[1] 詹三华[1] 高杉 WU Yang;WANG Xiu;ZHAN Sanhua;GAO Shan(People's Hospital of Tongling City,Tongling,Anhui,China 244000;School of Pharmacy,Anhui Medical University,Hefei,Anhui,China 230032)

机构地区：[1]安徽省铜陵市人民医院,安徽铜陵244000 [2]安徽医科大学药学院,安徽合肥230032

出　　处：《中国药业》2025年第3期57-62,共6页China Pharmaceuticals

基　　金：安徽省高校自然科学研究项目[KL2020A0860]。

摘　　要：目的探讨双参通脉颗粒(GSG)是否通过抑制细胞外活化蛋白激酶1/2-核因子-κB(ERK1/2-NF-κB)信号通路改善急性心肌梗死(AMI)模型大鼠的心肌损伤。方法将60只SD大鼠分为假手术组(A组,等量生理盐水),模型组(B组,等量生理盐水),阿托伐他汀组(C组,8 mg/kg),GSG低、中、高剂量组(D1组、D2组、D3组,5,10,15 g/kg),各10只。除A组外,其余各组大鼠通过左冠状动脉前降支结扎建造AMI模型,造模成功后24 h灌胃相应药物。检测各组大鼠的心功能;采用酶联免疫吸附试验(ELISA)法检测血清炎性因子,按试剂盒操作检测生化指标;分别采用2,3,5-氯化三苯基四氮唑(TTC)染色法、苏木精-伊红(HE)染色法、原位末端标记(TUNEL)法检测心肌梗死、病理损伤及细胞凋亡情况;采用免疫印迹(Western blot)法检测细胞凋亡与通路相关蛋白表达情况。结果与B组比较,D1组、D2组、D3组大鼠左心室收缩压(LVSP)、平均动脉压(MAP)、左心室内压上升最大速率(+dp/dt_(max))、B细胞淋巴瘤-2(Bcl-2)表达水平均显著升高(P<0.05),左心室内压下降最大速率(-dp/dt_(max))、左心室舒张末压(LVEDP)、肿瘤坏死因子-α(TNF-α)、单核细胞趋化蛋白1(MCP-1)、白细胞介素(IL)-6、IL-1β、肌钙蛋白I(cTnI)、肌酸激酶同工酶(CK-MB)、心肌梗死程度、心肌细胞凋亡率、胱天蛋白酶-3(caspase-3)、B淋巴细胞瘤2相关X蛋白(Bax)、p-ERK1、p-ERK2、NF-κB p65表达水平均显著降低(P<0.05)。结论GSG可能通过抑制ERK1/2-NF-κB信号通路改善AMI模型大鼠的心肌损伤。Objective To investigate whether Shuangshen Tongmai Granules can improve myocardial injury in acute myocardial infarction(AMI)model rats by inhibiting the extracellular signal-regulated kinases 1/2-nuclear factor-κB(ERK1/2-NF-κB)signaling pathway.Methods A total of 60 SD rats were divided into the sham operation group(group A,equal volume of phgsiological saline),model group(group B,equal volume of phgsiological saline),atorvastatin group(group C,8 mg/kg),and low-,medium-,and high-dose Shuangshen Tongmai Granules groups(groups D1,D2,D3,5,10,15 g/kg),with 10 rats in each group.Except for rats in group A,rats in the other groups were used to establish AMI models by ligating the left anterior descending coronary artery.At 24 h after successful modeling,corresponding drugs were administered by gavage.The cardiac function of rats in each group was detected.The serum inflammatory factors were detected by the enzyme-linked immunosorbent assay(ELISA),and biochemical indicators were detected according to the test kits.Myocardial infarction,pathological damage,and cell apoptosis were detected by the TTC staining method,hematoxylin eosin(HE)staining method,and TdT-mediated dUTP nick end labeling(TUNEL)method,respectively.The expression of apoptosis-related protiens and pathway-related proteins in cells was detected by the Western blot.Results Compared with those in group B,the left ventricular systolic pressure(LVSP),mean arterial pressure(MAP),maximal left ventricular pressure rising rate(+dp/dt_(max)),and expression levels of B-cell lymphoma 2(Bcl-2)significantly increased in groups D1,D2,and D3,while the maximal left ventricular pressure decreasing rate(-dp/dt_(max)),left ventricular end-diastolic pressure(LVEDP),tumor necrosis factor-α(TNF-α),monocyte chemoattractant protein-1(MCP-1),interleukin(IL)-6,IL-1β,cardiac troponin I(cTnI),creatine kinase-MB(CK-MB),degree of myocardial infarction,myocardial cell apoptosis rate,the expression levels of caspase-3,BCL2-associated X protein(Bax),p-ERK1,p-ERK2,and NF-κB p65 si

关 键 词：双参通脉颗粒 细胞外活化蛋白激酶1/2 核因子-κB 急性心肌梗死 心肌损伤 

分 类 号：R932[医药卫生—生药学] R285.5[医药卫生—药学]