SOD在缺血预处理保护大鼠肝脏缺血再灌注损伤中的作用

Activation of Superoxide Dismutase After Ischemic Precon ditioning in Ischemia-Reperfusion Injury of Liver of Rats

目的 :探讨超氧化物歧化酶 (superoxidedismutase ,SOD)在缺血预处理保护肝脏缺血再灌注损伤过程中的作用。方法 :应用大鼠部分肝脏缺血再灌注损伤模型 ,检测缺血预处理组 (IP组 )、缺血再灌注组 (I/R组 )及对照组 (C组 )大鼠血清丙氨酸转氨酶 (alaninetransaminase,ALT) ,门冬氨酸转氨酶 (aspartatetransaminase ,AST)及乳酸脱氢酶 (lactatedehydrogenase ,LDH)水平与肝脏病理组织学改变 ,测定其肝脏组织SOD水平的变化并与单纯缺血预处理组 (OIP组 )大鼠进行比较。结果 :IP组的肝脏损害虽较C组重 ,但明显较I/R组轻 ,其 3种血清生化酶均显著低于I/R组 ;OIP组肝组织的SOD水平 (2 14 .95± 2 4 .38)NU/mgprotein均显著高于IP组 (172 .4 3± 15 .2 3)、I/R组 (16 4 .0 3± 30 .0 8)与C组 (16 7.0 3± 2 7.6 0 )NU/mgprotein (P <0 .0 1)。结论 :缺血预处理对大鼠肝脏缺血再灌注损伤具有保护作用 。

﨩bjective: [WT5'BZ]Our aim was to investigate the ro le of superoxide dismutase (SOD) in ischemic preconditioning (IP) to protect liv er against ischemia reperfusion injury in a rat model. [WT5'HZ]Methods: [WT5' BZ]Male Wistar rats were divided into 4 groups. Rats in the OIP and IP groups un derwent 10 minute ischemia in left lateral hepatic lobe. After 10 minute recov ery, rats in OIP group were immediately killed, and rats in IP group were consec utively insulted to warm ischemia in the left lateral hepatic lobe for 40 minute s. The rats in I/R group received warm ischemia of the left lateral hepatic lobe for 40 minutes without ischemic preconditioning. The rats in control group rece ived only laparotomy. After 90 minute recovery, levels of aspartate transaminas e (AST), alanine transaminas (ALT),and lactate dehydrogenase (LDH) in serum, an d levels of SOD in liver tissue in each group were measured. Histologic changes of liver after reperfusion were also compared. [WT5'HZ]Results: [WT5'BZ]In OIP group, the level of SOD (NU/mg protein) in liver tissue was (214.95±24.38), which was significantly higher than that in IP (172.43±15.23), I/R (164.03±30. 08), and control (167.03±27.60) groups(P<0.01). But there were no signifi cant difference among IP, I/R, and control groups. Although serum biochemical pa rameters (ALT, AST, and LDH) in IP group were higher than those in control group , they were significantly lower than those in I/R group. Compared with I/R group , tissue necrosis in IP group was prevented. [WT5'HZ]Conclusion: [WT5'BZ]The I P can protect liver from ischemia reperfusion injury, which was related to the activation of SOD in liver tissue, and SOD was consumed during its protective pr ocess by cleaning up free radicals.