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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.