热休克蛋白-70和一氧化氮在不同年龄大鼠肾缺血再灌注中的作用

The effect of HSP-70 and NO on renal ischemia reperfusion injury in young and aged rats

①目的探讨不同年龄大鼠肾缺血再灌注损伤(IRI)时热休克蛋白-70(HSP-70)和一氧化氮(NO)的变化及其作用机制。②方法夹闭双侧肾动、静脉45分钟后松夹再灌注。实验大鼠按鼠龄分为4组:青年大鼠对照组、青年大鼠缺血再灌注组、老年大鼠对照组、老年大鼠缺血再灌注组,每组均为6只。免疫组化法观察HSP-70表达,硝酸还原酶法测定血浆NO含量,双抗体夹心酶标免疫分析法测定血浆中iNOS水平。③结果青、老年IRI组大鼠HSP-70表达较对照组明显增强,肾小管上皮细胞胞浆内出现较多的棕黄色颗粒,呈弥漫性分布,肾小球未观察到明显棕黄色颗粒。青、老年IR组大鼠与对照组相比,血浆中NO含量升高而诱导型NO合酶(iNOS)含量下降。④结论HSP-70和NO保护肾脏对抗缺血再灌注损伤。HSP-70可能通过抑制iNOS的表达,从而直接或间接的促进了由原生型NO合酶(cNOS)诱导的具有保护作用的NO表达。

Objective To investigate the change and mechanisms of HSP -70 and NO in renal ischemia reperfusion injury （RIRI） in young and aged rats. Methods The model of RIRI was induced by bilateral damping the renal artery and vein for 45 min and followed by reperfusion. Young and aged rats were randomly divided into 4 groups （ n = 6 ） ： young control group （ YC ）, young ischemia reperfusion group（ YIR）, aged control group（ AC）, and aged ischemia reperfusion group（AIR）. The expression of HSP - 70 was observed by immunohistochemistry, the content of NO was determined with nitrate reductase method, and the level of iNOS was determined with double antibody sandwich enzyme label immune assay. Results The expressions of HSP - 70 in YIR and AIR group were high than those in YC and AC. A large number of brown particles were detected in the IR group in the renal tubular epithelial ceils and had a diffuse distribution, but which werent seen in the glomeruli. When compared with AC and YC group, the contents of NO in blood serum in AIR and YIR group were increased,while the contents of iNOS were reduced（ P 〈0.01）. Conclusion Kidney against the ischemia reperfusion injury was protected by HSP -70 and NO. HSP -70 possibly inhibited the ex- pression of iNOS and directly or indirectly promoted the expression of NO which was induced by cNOS.