热休克蛋白质70对大鼠肝脏缺血再灌注后NOS活力的影响

目的为探讨热应激预处理对肝脏缺血再灌注损伤的保护作用的机制,采用局部热应激处理诱导热休克蛋白质(HSP70)的表达,检测了HSP70对肝脏缺血再灌注时NOS活力的影响。方法将实验大鼠随机分为热应激预处理组与非预处理组,对比观察两组动物肝脏缺血再灌注后0、4、8、12、24h期间内肝脏HSP70的表达、NOS活力及血清乳酸脱氢酶(lactate dehydrogenase,LDH)的活性与肝脏组织学改变。结果热应激预处理组HSP70的表达水平均比非预处理组同一时间点高,而NOS活力及血清LDH的活性较非预处理组低。与非预处理组比较,经热应激预处理肝组织损伤较轻。结论热应激预处理诱导产生的热休克蛋白70保护肝脏缺血再灌注损伤的作用途径之一可能是通过抑制NO的产生,从而降低大量自由基对肝脏的损害。

Effects of HSP70 on the NOS Activity of Rat Liver after Ischemia Reperfusion

Objective To investigate the protective effect of heat stress pretreatment on the hepatic ischemia resperfusion (I/R) injury and its mechanism of action. Methods To establish the rat model of hepatic ischemia resperfusion injury using Pringle's maneuver with or without heat stress pretreatment. The rats were randomly divided into pretreatment group (HP+IR) and non-pretreatment group (IR). The activity of NOS in the liver, the activity of serum enzyme LDH and the pathological changes of the liver were assessed at 0, 4, 8, 12 and 24 h after I/R. Results At each time point set after I/R, the activity of NOS in the liver of HP+IR group was lower than that of IR group. Maximal HSP70 expression was observed at 12 h after heat pretreatment. While in the HP+IR group, the level of liver enzyme was significantly reduced and the pathological changes were improved in comparison with those in IR group. Conclusion HSP70 induced by heat pretreatment protects the liver against I/R injury may be through inhibiting the NOS activity and therefore reducing the insults of oxygen free radicals on the liver.