摘要
目的 观察热休克反应 (HSR)后 0、2 4、4 8、96、192h热休克蛋白 72 (HSP72 )表达水平的变化及再灌注后心肌组织SOD、CAT、MDA含量变化 ,探讨HSP72对缺血再灌注心肌保护的可能机制。方法 全身高温 4 2℃维持 15min制作热休克模型。各组心脏离体逆行灌注 ,常温下 (37℃ )缺血 2 5min ,再灌注 4 0min。测定缺血前、再灌注后心肌组织SOD、CAT、MDA含量 ,观察各组心肌HSP72表达。结果 再灌注后 2 4h和 4 8h两组心肌组织MDA含量减少 ,SOD、CAT活性明显高于对照组。对照组和热预处理后 0h几乎无HSP72表达 ,其表达高峰在热预处理后 2 4、4 8h ,随后逐渐降低 ,于 192h返回基线水平。结论 热休克蛋白能提高抗氧化酶活性 ,减轻心肌缺血再灌注损伤。
Objective To observe the changes of HSP72 expression and the content of myocardial MDA,SOD and CAT in 0,24,48,96 and 192 hours after hyperthermia. To discuss the possible mechanism of the protection of ischemic myocardium by HSP. Methods The rats were divided into six groups, namely, the control group and 0,24,48,96,192 hours HSR group. Rats were exposed to 42℃ hyperthermia for 15 min. After the hearts were isolated from control and hyperthermia treated rats and retrogradely perfused, they were subjected to normothermic global ischemia for 25 min followed by reperfusion for 40 min. Myocardial SOD,CAT,MDA was checked before ischemia and after reperfusion. Expression of HSP72 proteins in the myocardium was examined by immunohistochemical staining in each group. Results The content of myocardial MDA was higher in group control than group 24h and 48h . SOD and CAT activity was significantly increased in 24h and 48h postheat shock hearts. In group 24h and 48h, a large accumulation of HSP72 was detected. HSP72 then decreased and back to basal level at 192h after hyperthermia. Conclusion HSP 72 can protect the activity of antioxidases, and decrease the injury of reperfusion.
出处
《重庆医学》
CAS
CSCD
2002年第5期361-362,共2页
Chongqing medicine
