龙胆苦甙对减轻乳鼠心肌缺血再灌注损伤的细胞研究

被引：4

作者：

陈浩 ^{[1
]}

乔慧莲 ^{[2
]}

张磊 ^{[3
]}

肖丹 ^{[3
]}

陈赵云 ^{[3
]}

易定华 ^{[1
]}

机构：

[1] 第四军医大学西京医院心血管外科

[2] 第四军医大学人体解剖与组织胚胎学教研室

[3] 第四军医大学流行病学教研室

来源：

中华临床医师杂志(电子版) | 2013年 / 7卷 / 23期

关键词：

再灌注损伤; 龙胆苦甙; Akt/Gsk3β信号通路;

D O I：

暂无

中图分类号：

R285.5 [中药实验药理];

学科分类号：

1008 ;

摘要：

目的观察龙胆苦甙(Gentiopicroside,GPS)后处理对离体心肌细胞缺血/再灌注损伤(ischemia and reperfusion injury,I/R)的拮抗作用及其可能的机制。方法采用SD大鼠乳鼠培养心肌原代细胞,用缺氧复氧模型模拟缺血再灌注(stimulated ischemia reperfusion,SI/R)。实验分为正常对照组(Control+ScrambleRNA+Veh);缺氧复氧组(I/R+ScrambleRNA+Veh);缺氧复氧+龙胆苦甙后处理组(I/R+ScrambleRNA+GPS组)以及缺氧复氧+AktSiRNA+龙胆苦甙后处理组(I/R+AktSiRNA+GPS)。采用化学法缺氧复氧模型,缺氧2 h,复氧4 h。复氧前给予GPS药物,检测心肌细胞乳酸脱氢酶(LDH)以及TUNEL染色确定心肌细胞的损伤程度以及抑制Akt表达后GPS的保护作用变化。结果与I/R+ScrambleRNA+Veh组相比,I/R+ScrambleRNA+GPS组LDH明显降低(P<0.01),TUNEL染色阳性率增加减少(P<0.01),Akt/Gsk3β信号通路磷酸化程度明显增加(P<0.01)。与I/R+ScrambleRNA+GPS组相比,SI/R+SiAktRNA+GPS组,LDH活性显著增加(P<0.01),TUNEI染色阳性率增加(P<0.01),Gsk3β磷酸化程度减弱(P<0.01)。结论 GPS后处理对I/R大鼠心肌具有保护作用,其作用机制与AKT/Gsk3β信号通路的活化有关。

引用

页码：10731 / 10735

页数：5

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