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黄芪甲苷通过调节PI3K/AKT/GSK-3β信号通路减轻大鼠心肌缺血再灌注损伤。

Astragaloside IV alleviates myocardial ischemia-reperfusion injury in rats through regulating PI3K/AKT/GSK-3β signaling pathways.

作者信息

Wei Dajun, Xu Hongjie, Gai Xiaodong, Jiang Ying

机构信息

MD, Department of Cardiology, Affiliated Hospital, Beihua University, P.R. China. Technical procedures, acquisition of data, final approval.

Master, Department of Oncology, Affiliated Hospital, Beihua University, P.R. China. Design of the study, critical revision, final approval.

出版信息

Acta Cir Bras. 2019 Sep 12;34(7):e201900708. doi: 10.1590/s0102-865020190070000008.

Abstract

PURPOSE

To investigate the effect of astragaloside IV (As-IV) on myocardial ischemia-reperfusion (I/R) injury in rats and reltaed mechanisms.

METHODS

Sixty rats were randomly divided into sham-operated, control I/R and 2.5, 5 and 10 mg/kg As-IV groups, 12 rats in each group. The later three groups were intragastrically administered with As-IV for 7 days, with a dose of 2.5, 5 and 10 mg/kg, respectively. The myocardial I/R injury model was constructed in later four groups. At the end of reperfusion, the cardiac function indexes, serum lactate dehydrogenase (LDH) and creatine kinase (CK) levels, heart weight (HW)/body weight (BW) ratio and infarct size, and expressions of phosphatidylinositol-3 kinase/serine-threonine protein kinase (PI3K/AKT) and glycogen synthase kinase-3β (GSK-3β) proteins and the phosphorylated forms (p-AKT, p-GSK-3β) were determined.

RESULTS

Compared with control I/R group, in 5 and 10 mg/kg As-IV groups the left ventricular systolic pressure, fractional shortening and ejection fraction were increased, the left ventricular end-diastolic pressure was decreased, the serum LDH and CK levels were decreased, the HW/BW ratio and myocardial infarct size were decreased, and the p-Akt/Akt ratio and p-GSK-3β/GSK-3β ratio were increased (all P < 0.05).

CONCLUSION

As-IV can alleviate the myocardial I/R injury in rats through regulating PI3K/AKT/GSK-3β signaling pathways.

摘要

目的

探讨黄芪甲苷IV(As-IV)对大鼠心肌缺血再灌注(I/R)损伤的影响及其相关机制。

方法

将60只大鼠随机分为假手术组、对照I/R组以及2.5、5和10mg/kg As-IV组,每组12只。后三组分别给予As-IV灌胃7天,剂量分别为2.5、5和10mg/kg。后四组构建心肌I/R损伤模型。再灌注结束时,测定心功能指标、血清乳酸脱氢酶(LDH)和肌酸激酶(CK)水平、心脏重量(HW)/体重(BW)比值和梗死面积,以及磷脂酰肌醇-3激酶/丝氨酸-苏氨酸蛋白激酶(PI3K/AKT)和糖原合酶激酶-3β(GSK-3β)蛋白及其磷酸化形式(p-AKT、p-GSK-3β)的表达。

结果

与对照I/R组相比,5和10mg/kg As-IV组左心室收缩压、缩短分数和射血分数升高,左心室舒张末期压力降低,血清LDH和CK水平降低,HW/BW比值和心肌梗死面积减小,p-Akt/Akt比值和p-GSK-3β/GSK-3β比值升高(均P<0.05)。

结论

As-IV可通过调节PI3K/AKT/GSK-3β信号通路减轻大鼠心肌I/R损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a2ea/6746565/416f882ba086/1678-2674-acb-34-07-e201900708-gf01.jpg

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