决明子提取物减轻2型糖尿病大鼠心肌缺血/再灌注损伤

被引：10

作者：

刘利兵 ^{[1
]}

张海锋 ^{[2
]}

机构：

[1] 西京学院医学护理教研室

[2] 第四军医大学教学实验中心

来源：

基础医学与临床 | 2015年 / 35卷 / 01期

关键词：

决明子; 糖尿病; 心肌缺血/再灌注损伤; Akt; ERK1/2;

D O I：

10.16352/j.issn.1001-6325.2015.01.001

中图分类号：

R259 [现代医学内科疾病];

学科分类号：

100506 ;

摘要：

目的研究决明子提取物(SCE)对糖尿病大鼠心肌缺血/再灌注(MI/R)损伤的影响。方法构建高脂饲料-链脲霉素诱导的2型糖尿病大鼠模型(HFD-STZ),大鼠随机分为对照组(Con)、SCE处理组(Con+SCE,每日灌胃给予SCE,10 mg/kg)、糖尿病组(DM)和糖尿病SCE处理组(DM+SCE)。1周后行心肌缺血30 min/再灌注4或6 h,并检测血浆总胆固醇(TC)和三酰甘油(TG)水平,用伊文氏蓝-TTC法检测心肌梗死范围、用试剂盒检测血清肌酸激酶(CK)和乳酸脱氢酶(LDH)活性、用TUNEL法和caspase-3试剂盒检测细胞凋亡,用Western blot法检测Akt、ERK1/2表达及磷酸化等。结果 HFD-STZ大鼠MI/R损伤加重,虽SCE处理1周对正常动物MI/R损伤无影响,但降低HFD-STZ大鼠TC、TG水平,可将其心肌梗死面积减小至38.4%±2.7%,显著低于糖尿病组的46.1%±3.2%(P<0.05),且血清CK、LDH活性及细胞凋亡减少;还可增加HFD-STZ大鼠心肌Akt及ERK1/2磷酸化。用Akt或ERK1/2抑制剂可阻断SCE的心肌保护作用。结论 SCE可有效减轻糖尿病大鼠MI/R损伤,可能与其降脂并激活Akt及ERK1/2信号有关。

引用

页码：1 / 6

页数：6

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