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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 effect of taurine on hepatic function after limb ischemia-reperfusion in experimental rats and its possible mechanism. Methods Wistar rats were randomly divided into ischemia-reperfusion group (model group), administration group and normal control group. Ischemia-reperfusion group was used to block the experimental model of blood flow duplication in both hind legs. The medication group was fed with taurine 200 mg / kg body weight 30 days before the experiment, then the model was duplicated. Normal control group rats without any treatment. The levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), xanthine oxidase (XOD) and superoxide Activity of dismutase (SOD). Results The ALT in the model group was (4.70 ± 0.38) U / L, AST (2.86 ± 0.27) U / L, and XOD was (45.53 ± 9.09) U / L and significantly higher than that in the normal control group (1.23 ± 0.22 U / L , AST (1.51 ± 0.17) U / L and XOD (32.62 ± 2.61) U / L were also higher than those of the treated group (3.86 ± 0.54 U / L, AST 36.23 ± 3.25) U / L. The level of SOD in ischemia-reperfusion group was (77.98 ± 8.96) U / L, which was significantly lower than that in normal control group (107.97 ± 9.60) U / L and that in treated group (89.98 ± 10.19) U / L The differences were statistically significant (P <0.01 or P <0.05). Conclusion Taurine can reduce liver injury induced by ischemia-reperfusion injury in rats. The mechanism may be related to the anti-oxidative response of the body after ischemia-reperfusion to avoid or delay the occurrence and development of limb ischemia-reperfusion injury.