摘要
目的:通过研究开环异落叶松树酯酚二葡萄糖苷(SDG)对心肌缺血再灌注去卵巢大鼠心脏组织磷脂酰肌醇3-激酶/蛋白激酶B/内皮型一氧化氮合酶(PI3K-Akt-eNOS)的影响,探讨SDG对心肌缺血再灌注损伤的保护机制。方法:100只SD雌性大鼠随机分为去卵巢组、缺血再灌注假手术组、缺血再灌注组、雌二醇干预组和SDG干预组。SDG干预组以50mg·kg^(-1)·d^(-1)剂量灌胃,雌二醇干预组以0.8mg·kg^(-1)·d^(-1)剂量灌胃,其余组均以等量蒸馏水灌胃。伊文氏蓝和2,3,5-氯化三苯基四氮唑双染色法测定心肌梗死面积,ELISA双抗体夹心法检测雌激素水平变化,Western blot法测定PI3K、Akt、eNOS以及三者磷酸化蛋白以及雌激素受体α(ERα)蛋白的表达。结果:SDG干预60d后,雌二醇干预组和SDG干预组雌激素水平显著高于缺血再灌注组,而心肌梗死区面积百分比显著低于缺血再灌注组(P<0.05)。此外,雌二醇干预组和SDG干预组中p-PI3K、p-Akt、peNOS和ERα4种蛋白的表达均显著高于缺血再灌注组(P<0.05)。结论:SDG可能通过激活雌激素受体α,活化PI3K-Akt-eNOS信号通路,从而对去卵巢大鼠心肌缺血再灌注损伤发挥保护作用。
Objective：To investigate the mechanism of the cardio-protection of SDG on MIRI through the effect of SDG on PI3K-Akt-eNOS signaling pathway in ovariectomized MIRI rats.Method：The 100 SD female rats were divided into 5groups：OVXsham,MIRIsham,MIRI,estradiol treated（EST）and SDG treated.In the group of SDG treated,ovariectomized rats were perfused at a dose of 50mg/（kg·d）,while the EST selected a dose of 0.8mg/（kg·d）.Otherwise the other three groups just used distillation water.We determined the infarcted sizes in heart with Even＇s Blue-TTC analysis,and detected the estrogen level by ELISA analysis.The expression of ERα,phospho-PI3 K,phosphor-Akt,phosphor-eNOS protein were tested in myocardium through western blot analysis.Result：After 60 days of SDG intervention the estrogen level in EST treated group and SDG treated group were significantly higher than MIRI group（P0.05）.In addition,the myocardial infarction area of EST treated group and SDG treated group were significantly poorer than MIRI group（P0.05）.Finally the p-PI3 Kand p-Akt and peNOS and ERαprotein of myocardium were expressed at higher level in SDG treated group and EST treated group than in MIRI group.Conclusion：As a result,it could be inferred that the cardio-protection mechanism of SDG on injury of MIRI in ovariectomized rats might lie in the process in which the ERαtouched off by SDG to activate PI3K-Akt-eNOS signaling pathway.
出处
《临床心血管病杂志》
CAS
CSCD
北大核心
2016年第8期848-852,共5页
Journal of Clinical Cardiology
基金
山西省基础研究项目(No:2013011049-5)
