芪桂益脉灵干预急性心肌缺血再灌注大鼠模型炎症因子ICAM-1,VCAM-1和p38MAPK通路的实验研究  

Experimental Study of Qigui Yimailing on ICAM-1,VCAM-1 and p38 Pathway in Rat Models with Acute Myocardial Ischemia-reperfusion Injury

作　　者：赵龙[1] 徐京育[2] 张超越[1] 臧萌[3] 

机构地区：[1]黑龙江中医药大学,黑龙江哈尔滨150040 [2]黑龙江中医药大学附属第一医院,黑龙江哈尔滨150040 [3]佳木斯大学医学院,黑龙江佳木斯154007

出　　处：《中医药信息》2017年第3期51-54,共4页Information on Traditional Chinese Medicine

基　　金：黑龙江省自然科学基金项目(No.H201326)

摘　　要：目的:观察芪桂益脉灵(QGYML)对大鼠急性心肌缺血再灌注损伤模型血管细胞黏附因子-1(VCAM-1)和内皮细胞间黏附分子-1(ICAM-1),p38MAPK通路的影响。方法:50只大鼠随机分为空白组、假手术组、单纯缺血再灌注组、QGYML低剂量组、QGYML高剂量组5组,灌胃1 h后,结扎左冠状动脉前降支,结扎60 min,再灌注180 min,测定VCAM-1、ICAM-1、p38、p-p38蛋白表达。结果:各组p38蛋白表达基本一致,差异无统计学意义(P>0.05);单纯缺血再灌注组与假手术组比较,VCAM-1、ICAM-1、p-p38蛋白表达升高(P<0.05),差异有统计学意义;灌药组与单纯缺血再灌注组比较,VCAM-1、ICAM-1、p-p38蛋白表达明显降低(P<0.05),差异有统计学意义,高剂量组效果更佳。结论:芪桂益脉灵可以下调VCAM-1和ICAM-1在内皮细胞膜上的表达,抑制p38MAPK通路,对急性心肌缺血再灌注损伤有抑制作用。Objective： To study the effect of QGYML on ICAM - 1, VCAM - 1 and p38 pathway in rat models with acute myocardial ischemia -reperfusion injury. Methods ：50 SD male rats were randomly divided into nor- mal group （ N）, sham operation group （ SH ）, pure ischemia reperfusion group （ I/R）, QGYML low dose group （QL） and QGYML high dose group（QH）. Fill the stomach after one hour; ligate the left anterior descending artery for 60 minutes with 180 minutes of reperfusion; determine VCAM 1, ICAM - 1, p38 and p -p38 pro- tein expressions. Results ： There was no statistically significant difference of p38 （ P 〉 0.05 ）. I/R group was compared with SH group and VCAM - 1, ICAM - 1 and p - p38 expressions were increased. Compared with I/Q, in QGYML group VCAM - 1, ICAM - 1 and p - p38 were decreased significantly （ P 〈 0.05 ）, and the effect of QH was better. Conclusion：QGYML can cut VCAM - 1 and ICAM - 1 in endothelial cell membranes, inhibit p38MAPK pathway and inhibit acute myocardial ischemia -reperfusion injury.

关 键 词：芪桂益脉灵 细胞间黏附分子-1 血管细胞黏附分子-1 再灌注损伤 P38丝裂原活化蛋白激酶 

分 类 号：R285.5[医药卫生—中药学] R-332[医药卫生—中医学]