依达拉奉对实验性肝纤维化大鼠脂质过氧化的影响

目的探讨依达拉奉（EDA）对实验性肝纤维化大鼠脂质过氧化的影响。方法以四氯化碳诱导大鼠肝纤维化模型。30只Sprague—Dawley大鼠随机分为对照组（10只）、肝纤维化模型组（10只）和EDA防治组（10只）。检测各组大鼠血清谷丙转氨酶、谷草转氨酶水平及肝组织羟脯氨酸、丙二醛含量和超氧化物歧化酶活性。结果EDA防治大鼠血清谷丙转氨酶和谷草转氨酶水平分别为714．2±28．2U／L和766．0±11．0U／L，较模型组（1110．3±45．9U／L和1640．3±26．7U／L，P〈0．05和P〈0．01）明显降低；EDA组大鼠肝组织羟脯氨酸和丙二醛含量分别为0．4±0．1μg／mg和5．5±2．3nmol／gl，较模型组（0．8±0．1μg／mg和7．5±2．1nmol／gl，P均〈0．01）显著下降；EDA组大鼠超氧化物歧化酶活性为129．7±2．3u／g，较模型组（933±3．9u／g，P〈0．01）明显升高；EDA组和模型组大鼠肝组织纤维化评分分别为2．7±1．0和3．5±0．7，差异显著（P〈0．01）。结论EDA对大鼠肝纤维化有一定的防治作用，其机制很可能与抗脂质过氧化损伤有关。

Effect of edaravone on lipid peroxidation in rats with CCl4-induced liver fibrosis

Objective To investigate the effect of edaravone on lipid peroxidation in rats with CC14-induced liver fibrosis. Methods Liver fibrosis model in rats was established by carbon tetraehloride injection. Thirty Sprague-Dawley rats were randomly divided into normal （n=10）,fiver fibrosis （n=10）and edaravone-treated group （n=10）. Serum aspartatc aminotransferase and alanine aminotransferase levels were assessed,and liver hy-droxyproline,malondialdehyde contents and superoxide dismutase activity were determined. Results Liver fibrosis model was established successfully. In edaravone group,serum aspartate aminotransferase and alanine aminotransferase levels were714.2±28.2U/L and 766.0 ±11 .0U/L, respectively , obviously reduced as compared with in model group （1110.3±45.9U/L and 1640.3±26.7U/L,P〈0.05 and P〈0.01 ）;Liver contents of hydroxyproline and malondi- aldehyde in edaravone group were 0.43±0.09txg/mg and 5.5 ±2.3nmol/gl,respeetively,significantly decreased as compared with in model group （0.76±0.12μg/mg and 7.5±2.1nmol/gl,P〈0.01）;While superoxide dismutase activity in edaravone group were 129.7±2.3u/g,significantiy increased as compared with in model group （93.3±3.9u/g,P〈0.0l）; The score of liver fibrosis in edaravone group was 2.7±1.0,mueh lower than in model group （3.5±0.7,P〈0.01）. Conclusion Edaravone has a therapeutic effect on liver fibrosis in rats,and the mechanism is possibly related to the alleviation of liver injury induced by lipid peroxidation.