摘要
目的:观察三七预处理对大鼠心肌缺血再灌注损伤的保护作用。方法:70只成年雄性SD大鼠随机数字表法分成4组:空白对照组、缺血再灌注组、缺血预适应组、三七预处理组,建立在体心肌缺血再灌注动物模型。采用NBT染色法检测心肌梗死面积、全自动生化分析仪检测血浆乳酸脱氢酶(LDH)、肌酸激酶同工酶(CK-MB)含量,免疫组化法观察蛋白激酶-α(PKC-α)蛋白表达。结果:①与空白对照组比较:缺血再灌注组、缺血预适应组、三七预处理组心肌酶CK-MB,LDH和心肌梗死面积显著增高(P<0.01),PKC-α蛋白表达增高(P<0.01)。②与缺血再灌注组比较:缺血预适应组、三七预处理组心肌酶CK-MB和LDH含量降低,心肌梗死面积显著减小(P<0.01),PKC-α蛋白表达增高(P<0.01)。③缺血预适应组与三七预处理组比较:心肌梗死面积、心肌酶(CK-MB和LDH)含量和PKC-α蛋白表达组间均无统计学差异(P>0.05)。结论:三七预处理能够减少心肌酶CK-MB和LDH含量,减少心肌梗死面积,上调PKC-α蛋白表达,发挥对缺血再灌注心肌的保护作用。
Objective: To investigate protective effect of Panax Notoginseng preconditioning on ischemic/ reperfusion (I/R) injury in rat hearts. Methods: SD male rats (n = 70) were randomly divided into 4 groups with 10 rats in each group. I/R injury was induced in isolated hearts, and the effect of Panax Notoginseng preconditioning was evaluated. Myocardial infarct size was detected by nitroblue tetrazolium staining; MB isoenzyme of ereatine kinase (CK-MB) and lactate dehydrogenase (LDH) activity were measured by automatic biochemistry analyzer; the expression of protein kinase C-α (PKC-α) was detected by immunohistochemical method. Results: (1) Compared with control, the CK-MB, LDH and myocardial infarct size were significantly increased (P 〈 0.01 ) , but PKC-α expression was reduced (P 〈 0.01 ) in groups with ischemie preconditioning, I/R injury, Panax Notoginseng treatment. (2) Compared with I/R, CK-MB, LDH and myocardial infarct size were significantly reduced (P 〈 0.01) ; PKC-α expression was increased (P 〈0.01). (2) Compared with Panax Notoginseng and IP groups, CK- MB, LDH and myocardial infarct size as well as PKC-α expression did not change significantly (P 〉 0.05). Conclusion: Preconditioning with Panax Notoginseng reduces CK-MB, LDH and myocardial infarct size, and increases PKC-α expression; indicating that it protects rat myocardium from I/R injury.
出处
《中国新药杂志》
CAS
CSCD
北大核心
2009年第8期737-740,共4页
Chinese Journal of New Drugs
关键词
心肌缺血再灌注损伤
心肌缺血预适应
三七预处理
蛋白激酶C
myocardium ischemia/reperfusion injury
ischemic preconditioning
Panax Notoginseng preconditioning
PKC-α