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机构地区:[1]民航总医院康复体检中心,北京市100123 [2]首都医科大学附属北京同仁医院消化内科
出 处:《实用肝脏病杂志》2013年第1期63-65,共3页Journal of Practical Hepatology
摘 要: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(93.3±3.9 u/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。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.
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