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作 者:周剑寅[1,2] 尹震宇[1,2] 王生育[3] 颜江华[3] 赵一麟[1,2] 吴端[1,2] 刘争进[4] 张盛[1,2] 王效民[1,2]
机构地区:[1]厦门大学附属中山医院肝胆外科,福建厦门361004 [2]厦门市消化疾病诊治中心,福建厦门361004 [3]厦门大学医学院抗癌研究中心,福建厦门361005 [4]厦门大学附属中山医院病理科,福建厦门361004
出 处:《药学学报》2012年第11期1483-1488,共6页Acta Pharmaceutica Sinica
基 金:国家重大传染病防治科技重大专项"十二五计划"(2012ZX10002-011-005);国家自然科学基金面上项目(81171976);福建省卫生厅中医药科研课题(wzy0904)
摘 要:探讨熊胆对二乙基亚硝胺(diethylnitrosamine,DEN)诱发大鼠肝癌的影响。将大鼠随机分为正常组、模型组及熊胆两个剂量组(200、400 mg.kg 1,灌胃18周,每周5次)。DEN诱发肝癌,用熊胆粉干预。实验观察了体重等一般情况,检测肝功能,HE染色观察肝组织病理改变,免疫组化检测肝组织中增殖细胞核抗原(PCNA)和平滑肌动蛋白(α-SMA)。结果显示:4周后正常组体重高于其他各组(P<0.01),熊胆两组均高于模型组(P<0.05);除正常组外,其余各组谷丙转氨酶、总胆红素显著升高,但熊胆两组显著低于模型组;模型组呈典型肝硬化、肝癌改变,熊胆两组肝硬化程度较轻、癌组织分化较好;模型组高表达PCNA和α-SMA,熊胆两组较模型组弱,α-SMA减少具有显著意义。实验提示:熊胆在一定程度上抑制了DEN诱发肝癌的进程,可能与抑制肝星状细胞活化并减轻肝损害、肝硬化有关。To investigate the influence of bear bile on rat hepatocarcinoma induced by diethylnitrosamine (DEN), a total of 40 rats were randomly divided into 4 groups: normal control group, model group, and two bear bile treatment groups. The rat liver cancer model was induced by breeding with water containing 100 mg L-1 DEN for 14 weeks. The rats of the bear bile groups received bear bile powder (200 or 400 mg-kg-1) orally 5 times per week for 18 weeks. The general condition and the body weight of rats were examined every day. After 18 weeks the activities of serum alanine transaminase (ALT), aspartate transaminase (AST) and total bilirubin (TBIL) were detected. Meanwhile, the pathological changes of liver tissues were observed after H&E staining. The expression of proliferative cell nuclear antigen (PCNA) and a-smooth muscle actin (a-SMA) in liver tissue were detected by immunohistochemical method. After 4 weeks the body weights of rats in normal group were significantly more than that in other groups (P 〈 0.05); and that in the two bile groups was significantly more than that in the model group. pyruvic transaminase and total bilirubin increased Compared with normal group, the level of serum glutamic- significantly in other groups; compared with model group, these two indexes decreased significantly in two bile groups. Hepatocellular carcinoma occurred in all rats except for normal group; there were classic cirrhosis and cancer in model group while there were mild cirrhosis and high differentiation in two bile groups. There were almost no expressions of PCNA and a-SMA in normal group while there were high expressions in model group; the two bile groups had some expressions but were inferior to the model group, and a-SMA reduced markedly of liver cancer during DEN inducing rat hepatocarcinoma, cell activation and relieving hepatic lesion and cirrhosis. R indicated that bear bile restrained the development which may be related to its depressing hepatic stellate cell activation and re
分 类 号:R963[医药卫生—微生物与生化药学]
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