实验性大鼠肢体缺血再灌注后肝脏损伤与牛磺酸的保护作用

Rat Liver Injury Induced by Limb Ischemia Reperfusion and Protective Effect of Taurine

目的探讨牛磺酸对实验性大鼠肢体缺血再灌注后肝脏功能的影响及其可能机制。方法实验用Wistar大鼠,随机分为缺血再灌注组(模型组),给药组和正常对照组。缺血再灌注组采用阻断双后肢血流复制实验模型,给药组于实验前30天灌服牛磺酸200 mg/kg体重,再复制模型。正常对照组大鼠不做任何处理。采用分光光度法分别测定模型组、给药组、对照组大鼠血浆中丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、黄嘌呤氧化酶(XOD)与超氧化物歧化酶(SOD)的活力。结果模型组ALT为(4.70±0.38)U/L、AST(2.86±0.27)U/L、XOD为(45.53±9.09)U/L,明显高于正常对照组ALT(1.23±0.22)U/L、AST(1.51±0.17)U/L和XOD(32.62±2.61)U/L,也高于给药组的ALT(3.86±0.54)U/L,AST(2.32±0.44)U/L和XOD(36.23±3.25)U/L。缺血再灌注组SOD为(77.98±8.96)U/L,明显低于正常对照组SOD(107.97±9.60)U/L及给药组的SOD(89.98±10.19)U/L,3组组间比较,差异均有统计学意义(P<0.01或P<0.05)。结论牛磺酸可以减轻试验大鼠缺血再灌注后所致肝脏损伤,其机制可能与其缺血再灌注后机体的抗氧化反应避免或延缓肢体缺血再灌注损伤的发生和发展有关。

Objective To investigate the effects of taurine on liver injury of rat induced by limb ischemia reperfusion and its possible mechanism. Methods Wistar rats were randomly divided into ischemia reperfusion group（model group）, treatment group and normal control group. Ischemia reperfusion group adopted double block replication model of hind-limb blood flow. The treatment group fed with 200 mg/kg body weight of taurine 30 days before the experiment, and then copied the model. No treatment in rats was conducted and taken as the normal control group. ALT, AST, XOD and SOD contents in rat plasma of various groups were measured by spectrophotometer. Results In model group ALT（4.70±0.38）U/L, AST （2.86±0.27）U/L, and XOD（45.53±9.09）U/L were significantly higher than those of the normal control group ALT（1.23±0.22）U/L, AST（1.51±0.17）U/L and XOD（32. 62±2.61）U/L, also higher than those of the treatment group（3.86±0.54）U/L, （2.32±0.44）U/L and（36.23±3.25）U/L. SOD（77.98±8.96） U/L of ischemia reperfusion group was significantly lower than that of the control group（107.97± 9.60）U/L and the treatment group （89.98 ± 10.19）U/L. The differences in-between 3 groups were all statistically signifieant（P〈0.01 or P〈0.05）. Conclusions Taurine might alleviate the livei＂ injury induced by isebemia reperfusion. Its mechanism might relate to anti-oxidation ability resulted after ischemia reperfusion causing the retardation and deceleration of the occurrence and development of limb ischemia reperfusion injury.