检索规则说明:AND代表“并且”;OR代表“或者”;NOT代表“不包含”;(注意必须大写,运算符两边需空一格)
检 索 范 例 :范例一: (K=图书馆学 OR K=情报学) AND A=范并思 范例二:J=计算机应用与软件 AND (U=C++ OR U=Basic) NOT M=Visual
作 者:靳雅玲[1] 罗伟生[1] 欧士钰[1] 覃浩[1] 孙旭锐[1]
出 处:《时珍国医国药》2012年第9期2197-2199,共3页Lishizhen Medicine and Materia Medica Research
基 金:广西壮族自治区卫生厅重点课题(No.2010052)
摘 要:目的研究荔枝核总黄酮(total flavone from Litchi Chinensis Sonn,TFL)对二甲基亚硝胺(DMN)肝纤维化大鼠肝细胞凋亡的影响及其作用机制。方法以二甲基亚硝胺腹腔注射制备大鼠肝纤维化模型,同时分别以高、低剂量的TFL灌胃6周进行干预治疗,HE及Masson染色观察肝纤维化程度,免疫组化二步法检测凋亡相关蛋白Bcl-2、Bax的表达。结果模型组大鼠肝组织中Bcl-2、Bax的表达较正常组均显著升高(P<0.01);TFL高、低剂量给药组Bcl-2的表达较模型组升高(P<0.05)、Bax表达较模型组降低(P<0.05);TFL高剂量组与低剂量组比较Bcl-2升高(P<0.05)、Bax显著降低(P<0.01)。结论 TFL抗肝纤维化的作用可能是通过上调Bcl-2、下调Bax的表达,抑制肝细胞的凋亡来实现的,且具有一定的量效关系。肝纤维化的严重程度与Bcl-2的表达负相关、Bax的表达正相关。Objective To study the effects of total flavone from Litchi Chinensis Sonn (TFL) on liver cell apoptosis of rats hepat-ic fibrosis and its mechanism of action. Methods Hepatic fibrosis of rats were established by intraperitoneal injection of dimeth-ylnitrosamine, then all the rats irrigated stomach with different doses of TFL for 6 weeks. After the experiment, HE and Masson staining were observed. The degree of liver fibrosis, apoptosis related proteins ( Bel - 2Bax) were detected with immunohistochemi- eal staining. Results The expression of Bel - 2 and Bax in the model group was significantly higher than in the normal group ( P 〈 O. 01 ). Different doses of TFL compare ed to model group increased expression of Bcl-2( P 〈 0.05 ) and reduced Bax( P 〈 0. 05 ). In high - dose of TFL, expression of Bcl - 2 ( P 〈 0.05 ) was higher and Bax( P 〈 0.01 ) was lower than low - dose group. Conclusion TFL resistance hepatic fibrosis role may be by up regulating the expression of Bcl - 2 and down - regulating Bax, in-hibiting the liver cell apoptosis to achieve. It also shows a certain dose - effect relationship. The severity of liver fibrosis is nega-tively correlatied with the ratio of Bcl-2 and positively with Bax.
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在载入数据...
正在链接到云南高校图书馆文献保障联盟下载...
云南高校图书馆联盟文献共享服务平台 版权所有©
您的IP:216.73.216.188