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目的 观察胆道梗阻后肝脏的自由基损伤和粉防己碱( Tet) 的保护作用。方法 复制大鼠胆道梗阻模型,每日给予 Tet 30 mg/kg 体重灌胃,动态观测肝组织丙二醛( M D A) 和超氧化物歧化酶( S O D) 含量及血清 T Bil、 A L T、 A L P、 G G T 含量。结果 胆道梗阻后,血清 T Bil、 A L T、 A L P、 G G T 水平逐渐升高,肝组织 M D A 含量逐渐升高, S O D 逐渐减少,各梗阻组与对照组比较, P< 0 .05 。各 Tet 治疗组与同时相梗阻组比较,血清 T Bil、 A L T、 A L P、 G G T 水平下降( P< 0 .05) ;肝组织 M D A 含量减少( P<0 .01) , S O D 含量升高( P< 0 .05) 。肝组织 M D A 含量与血清 A L T、 A L P 含量变化呈明显正相关,r 值分别为0 .949 和0 .843( P< 0 .01) 。结论 自由基损伤可能是胆道梗阻导致肝损害的重要机制之一, Tet对胆道梗阻所致肝损害有明显保护作用。
Objective To observe the liver injury of free radicals and the protective effect of tetrandrine (Tet) after biliary obstruction. Methods Rat model of biliary obstruction was reproduced. Tet (30 mg / kg body weight) was given intragastrically every day to observe the contents of malondialdehyde (MDA) and superoxide dismutase (SOD) and serum TBil in liver tissues. A L T, A L P, G G T content. Results After biliary obstruction, serum levels of TBil, A L T, A L P and G G T gradually increased, and the content of M D A gradually increased and S O D decreased gradually. Compared with the control group, P <0. 05. The levels of TBil, A L T, A L P and G G T in each Tet treatment group were significantly lower than those in the control group (P <0.05), while the levels of M D A in liver tissue were decreased (P <0.01) ), S O D content increased (P <0 .05). The content of M D A in liver tissue was positively correlated with the content of serum A L T and A L P, and the r values were 0 respectively. 949 and 0. 843 (P <0 .01). Conclusion Free radical damage may be one of the important mechanisms of hepatic injury caused by biliary obstruction. Tet may protect liver from biliary obstruction.