缺血预处理对缺血再灌注肝脏中HSP70表达的影响

目的 观察缺血预处理（IPC）对缺血再灌注大鼠肝脏中热休克蛋白70（HSP70）表达的影响。方法 利用大鼠肝脏缺血再灌注（ischemia reperfusion,I/R)损伤模型，比较不同次数的缺血预处理组与I／R组以及各预处理级璋血清谷丙转氨酶（ALT）、乳酸脱氢酶（LDH），肝组织中丙二醛（MDA）、过氧化物歧化酶（SOD）、一氧化氮（NO）含量，并观察了肝组织中酶的漏出和脂质过氧化物的形成减少，肝细胞抗氧自由基能力增强，血清及肝组织中NO含量升高。组织中PMNs浸润量降低，HSP70及iNOS蛋白及mRNA表达增多。结论 缺血预处理对肝脏I／R损伤有显著的保护作用。NO参与了缺血预处理对HSP70表达的正性调控过程。一次缺血10min再灌注10min是理想的肝脏缺血预处理方式。

Effect of expression of HSP70 on an ischemia reperfusion liver treated with ischemia preconditioning

Objective To study the molecular mechanism of preconditioning on liver ischemia reperfusion(I/R) injury by examining the expression of heat shock protein 70. Method The rat hepatic ischemia reperfusion model was used to evaluate the levels of plasma alanine transaminase(ALT),lactate dehydrogenase(LDH),nitric oxide(NO),superoxide dismute(SOD) and the levels of hepatic NO, the numbers of polymorphonuclear cells (PMNs), the expression heat shock protein and inducible nitric oxide synthase(iNOS) mRNA. Results In preconditioning groups, leakage of enzymes and production of lipid peroxidation decreased, while the ability of PMNs in the radicals,and NO in plasma and in liver both increased. Infiltration of PMNs in the liver increased. The level of heat shock protein 70 and the level of iNOS mRNA enhanced. Conclusion Preconditioning significantly protects liver from ischemia reperfusion injury. NO may be involved in regulation of preconditioning on the expression of heat shock protein 70. It produces better protection on liver I/R injury that 10 min ischemia was followed by 10 min reperfusion.