首页|蒙古黄芪总黄酮通过下调NF-κB和p38 MAPK信号通路改善急性心肌梗死小鼠炎症反应

蒙古黄芪总黄酮通过下调NF-κB和p38 MAPK信号通路改善急性心肌梗死小鼠炎症反应

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目的 探讨蒙古黄芪总黄酮(total flavonoids of astragalus,TFA)通过下调NF-κB和p38 MAPK信号通路改善急性心肌梗死小鼠心肌炎症.方法 采用随机数字表法将40只C57 BL/6J小鼠随机分为假手术组、模型组、蒙古黄芪总黄酮组、美托洛尔阳性药组,冠状动脉左前降支结扎建立急性心肌梗死模型,小鼠连续灌胃给药10 d后,进行小鼠心电图、血清生化和HE染色;Western blotting检测小鼠心肌组织中NF-κB p65、p38 MAPK/p-p38 MAPK、TNF-α和JAK1/STAT1的蛋白表达.结果 急性心肌梗死小鼠经TFA治疗后,小鼠心电图PR区间波动正常,QT区间ST段微压低,T波并未倒置、血清肌酸激酶MB型同工酶(CK-MB)和肌红蛋白(MYO/MB)表达水平下调、心肌组织损伤程度明显减轻,细胞破裂减少,只有局部散在的炎性细胞浸润.Western blotting结果表明,通过TFA药物治疗后,JAK1、STAT1、NF-κB p65、TNF-α和p38 MAPK/p-p38 MAPK的蛋白表达量呈明显下降趋势.结论 TFA可减轻小鼠急性心肌梗死损伤,其作用可能是通过抑制NF-κB和p38 MAPK信号通路,减轻心肌炎症,进而改善心肌梗死.
Astragalus flavones improved the inflammatory response of mice with acute myocardial infarction by down-regulating NF-κB and p38 MAPK signaling pathways
Objective To investigate the improvement of myocardial inflammation in mice with acute myocardial infarction by down-regulation of NF-κB and p38 MAPK signaling pathways by total flavonoids of astragalus (TFA)in Mongolia.Methods Forty C57BL/6J mice were randomized into Sham group,model group,TFA group,and metoprolol-positive drug group by random number column method,and the left anterior descending branch of coronary artery was ligated to establish an acute myocardial infarction model,and the mice were given the drug by continuous gavage for 10 days.Then electrocardiograms of the mice,biochemistry of the serum,and HE staining were carried out;and the protein expression of NF-κB p65,p38 MAPK/p-p38 MAPK,TNF-α,and JAK1/STAT1 in the myocardial tissues of mice was detected by western blotting.Results After acute myocardial infarction mice were treated with TFA,the fluctuation of PR interval of mouse ECG was normal,the ST segment of QT interval was slightly depressed,the T wave was not inverted,the expression level of serum creatine kinase MB isoenzyme (CK-MB)and myoglobin (MYO/MB)was down-regulated,and the degree of damage to myocar-dial tissues was significantly reduced,with a decrease in cell rupture,and only a localized and scattered infiltra-tion of inflammatory cells.The results of western blotting showed that the protein expression of JAK1,STAT1,NF-κB p65,TNF-α,and p38 MAPK/p-p38 MAPK tended to decrease significantly after treatment by TFA drugs.Conclusion TFA attenuates acute myocardial infarction injury in mice,which may act by inhibiting the NF-κB and p38 MAPK signaling pathways,reducing myocardial inflammation and thus ameliorating myocardial infarction.

myocardial infarctiontotal flavonoids of astragalusinflammationnuclear transcription factor κBmitogen-activated protein kinase

孙雨婷、王羽

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内蒙古民族大学 公共卫生学院,内蒙古 通辽 028000

遵义医科大学 基础药理教育部重点实验室暨特色民族药教育部国际合作联合实验室,贵州 遵义 563006

心肌梗死 蒙古黄芪总黄酮 炎症 核转录因子-κB 丝裂原活化蛋白激酶

2024

遵义医科大学学报
遵义医科大学

遵义医科大学学报

CSTPCD
ISSN:2096-8159
年,卷(期):2024.47(12)