摘要
目的：探讨热休克反应对大鼠缺血-再灌心肌保护作用的可能机制。方法：SD大鼠，随机分为对照组及热休克组，动物经热休克处理恢复2或24h后复制缺血再灌模型并进行各项检测。结果：①热休克处理后心肌组织内SOD活性显著高于对照组，MDA含量则显著低于对照组。②热休克组心肌组织内乳酸及ATP含量均显著高于对照组，糖原含量则显著低于对照组。③热休克反应能诱导HSP70i的转录。结论：热休克反应对缺血-再灌心肌的保护作用与心肌能量代谢的改善、抗氧化能力的增强以及HSP70i的转录合成增强有关。
To explore mechanism of heat-shock (HS) response could protect ischedria/reperfusion rat heart invitro and in vivo.METHODS: SD rats, randomly allocated into heat shock group and control group. The follwing parame-ters were examined: SOD and MDA, glycogen, lactic acid and ATP, Northem dot blot of inducible heat shock pro-tein (HSP70i). RESULTS: The SOD activity of HS group is significantly higher than that of control group, and the MDAconentration of HS group is significantly lower than that of contol group.The concentration of lactic acid and ATP of HSgroup are sigmficantly higher than that of control group, and the concentiation of glycogen of HS group is significanily lowerthan that of control group. The results of HSP70i mRNA Northem dot blot sugnted that HSP70i gene of left ventricularof HS group expressed obviously at 2 hours afer heat shock. After 24 hours of recovery, no detectable expression could beseen in HS group; while the control group was negative after 2 or 24 hours of recovery. CONCLUSION : The protechvemechanism of heat shock rcsponse on ischemia and reperfusion injury may be related to the improving of antioxidation and en-ergy metabolism and the increased expression of HSP70i gene.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1999年第10期868-870,共3页
Chinese Journal of Pathophysiology
基金
国家卫生部科研课题!94-2-055
关键词
再灌注损伤
心肌缺血
热休克反应
大鼠
Heat
Shock
Reperfusion injury
Energy metabolism
Free radicals
