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作 者:曲颖[1] 宗蕾[1] 沈镭[2] 王燕[1] 徐铭益[1] 刘梅[1] 窦爱霞[1] 陆伦根[1]
机构地区:[1]上海交通大学附属第一人民医院消化内科,200080 [2]上海交通大学医学院附属仁济医院消化内科上海市消化疾病研究所
出 处:《胃肠病学》2011年第4期196-201,共6页Chinese Journal of Gastroenterology
基 金:上海市重点学科建设项目(No.Y0205)资助
摘 要:背景:前期体外实验发现肝苏具有肝细胞保护、抗氧化、抗肝纤维化作用。目的:探讨肝苏对实验性大鼠肝纤维化的防治作用。方法:以四氯化碳(CCl4)诱导大鼠肝纤维化模型。63只Sprague-Dawley(SD)大鼠随机分为正常对照组(7只)、肝纤维化模型组(14只)、低剂量肝苏干预组(1 g/kg,14只)、中剂量肝苏干预组(2 g/kg,14只)、高剂量肝苏干预组(4 g/kg,14只)。检测各组大鼠血清肝生化指标和透明质酸(HA)水平以及肝组织丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性,HE和Masson染色观察肝组织纤维化程度,免疫组化染色检测肝组织肝星状细胞(HSC)活化标记α-平滑肌肌动蛋白(α-SMA)以及Ⅰ型、Ⅲ型胶原含量。结果:大鼠肝纤维化模型建立成功。各剂量肝苏干预组血清ALT、AST、ALP、HA水平较模型组不同程度地下降;肝组织MDA含量较模型组下降,高、中剂量组差异显著,但SOD活性无明显变化;肝组织纤维化程度较模型组改善,尤以高剂量组为著;肝组织α-SMA、Ⅰ型、Ⅲ型胶原含量较模型组减少,前两者减少更为明显。结论:肝苏能减轻实验性大鼠肝纤维化的肝细胞损伤,降低肝组织MDA含量,抑制HSC活化和肝内胶原合成,具有抗氧化和抗纤维化作用。Preliminary study has shown that Gansu possesses the hepatocellular protective, antioxidant and antifibrotic effects in vitro. Aims: To assess the preventive and therapeutic effect of Gansu on rat experimental liver fibrosis. Methods: Rat liver fibrosis model was induced by carbon tetrachloride (CC14) treatment. Sixty-three SpragueDawley (SD) rats were randomly divided into normal control group (n=7), liver fibrosis model group (n=14), low-dose Gansu intervention group (1 g/kg, n=14), moderate-dose Gansu intervention group (2 g/kg, n=14) and high-dose Gansu intervention group (4 g/kg, n=14). Serum levels of biochemical markers of hepatic function and hyaluronie acid (HA) were assessed, hepatic malondialdehyde (MDA) content and superoxide dismutase (SOD) activity were determined. Liver fibrosis was evaluated by HE and Masson staining. Expressions of eL-smooth muscle aetin (c^-SMA), the biomarker of hepatic stellate cell (HSC) activation, as well as collagens I and m were determined by immunohistochemistry. Results: Rat liver fibrosis model was established successfully. Compared with liver fibrosis model group, senml levels of AI,T, AST, ALP and HA were reduced with various degrees in Gansu intervention groups. Hepatic content of MDA decreased, particularly in high- and moderate-dose Gansu intervention groups, while no significant difference in SOD activity was found. Liver fibrosis was ameliorated, especially in high-dose Gansu intervention group. Hepatic expressions of a-SMA, collagens I and m decreased, especially for the first two. Conclusions: Gansu ameliorates hepatocyte injury, reduces hepatic content of MDA, and inhibits the activation of HSC and the synthesis of collagens, thus having antioxidant and antifibrotic effects on experimental liver fibrosis in rats.
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