亚砷酸钠诱导HSP 72在大鼠肝脏热缺血–再灌注损伤中的保护作用

The Protective Effect of HSP 72Induced by Sodium Arsenite in Warm IschemiaReperfusion Injury of the Murine Liver.

目的:观察亚砷酸钠(SA)诱导大鼠肝脏产生热休克蛋白72(HSP72)的过程及其抗肝脏热缺血-再灌注损伤的作用。材料与方法:将24只SD大鼠随机分成SA组(预先给予SA6mg/kg)和对照组(预先给予生理盐水)。24h后,两组均阻断肝脏中、左叶血供60min,再灌注3、6h;分别用Westernblot检测肝脏中的HSP72表达;外周血测定ALT、AST、LDH;组织学作HE染色、免疫组化测定HSP72。结果:注射SA6mg/kg后12h肝脏开始产生HSP72,24h达到高峰,并持续至60h。肝脏热缺血60min再灌注3、6h后,SA组HSP72显著表达,血清ALT、AST、LDH显著下降(P<0.05),组织学检查显示肝脏损伤明显减轻。结论:SA可诱导大鼠肝脏产生HSP72;SA预先诱导肝脏产生对HSP72可使肝脏抵御热缺血鄄再灌注损伤。

Objective:To observe the induction of heat shock protein72(HSP72)production and its protective effect in warm ischemiareperfusion injury in the rat liver.Methods:Twenty-four SD rats were divided randomly into2groups:Group SA injection of SA(6mg per kg weight)and Group NS(injection of NS).After24hours,the rats underwent60minutes of temporary occlusion of the median and left,hepatic lobe vasculature followed by reperfusion for3and6hours.Expression of HSP72was monitored by Western blot;ALT,AST and LDH were determined in the peripheral blood;routine HE and immunohistochemical staining for HSP72were performed.Results:After injection of SA6mg per kg weight,the liver tissue began to express HSP72after12hours,and reached a higher level after24hours which was maintained for60hours.After60minutes of warm ischemia,followed by3and6h of reperfusion,significant expression of HSP72was observed in Group SA,which serum ALT,AST and LDH also descended significantely as compared to Group NS(P<0.05).Hepatic damage was alleviated notably as shown by histological staining.Conclusions:1.Sodium Arsenite can induce HSP72production in the rat liver;2.Preinduction of HSP72production by sodium Arsenite can enhance the resistance of the liver to warm ischemia-reperfusion injury.