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作 者:徐卫权 李艳 XU Weiquan;LI Yan(Department of Pharmacy,Yiling Hospital of Yichang City,Hubei Province,Yichang 443100,China)
机构地区:[1]湖北省宜昌市夷陵医院药剂科,宜昌443100
出 处:《医药导报》2019年第2期163-166,共4页Herald of Medicine
基 金:湖北省重大科学技术成果(EK010175)
摘 要:目的观察冷饭团对实验性肝纤维化大鼠肝组织Bcl-2、Bax及增殖细胞核抗原(PCNA)表达的影响,探讨其抗肝纤维化的作用机制。方法将60只SD大鼠随机分为正常对照组、模型对照组、秋水仙碱组和冷饭团小剂量组(2.5 g·kg-1)、冷饭团大剂量组(5 g·kg-1),每组12只。除正常对照组外,其余各组均采用四氯化碳和高脂低蛋白等复合因素诱导大鼠实验性肝纤维化。于造模后第2天开始给药,至第6周末结束。取肝组织做苏木精-伊红(HE)及Masson染色,观察肝纤维化程度,并采用免疫组织化学法检测肝组织中Bcl-2、Bax和PCNA蛋白的表达。结果冷饭团能明显减轻实验性肝纤维化大鼠肝组织损伤和肝纤维化程度。与模型对照组比较,冷饭团大、小剂量组和秋水仙碱组大鼠肝组织中Bax蛋白的表达明显降低,PCNA的表达明显升高(P<0.05或P<0.01)。结论冷饭团抗肝纤维化的机制可能与其影响肝组织中Bax和PCNA的表达来调节肝细胞的凋亡和增殖有关。Objective To observe the effect of Kadsura coccinea on the expression of Bcl-2,Bax and proliferating cell nuclear antigen(PCNA)in liver tissue of experimental hepatic fibrosis rats,to further discuss the mechanism of anti-liver fibrosis.Methods Sixty SD rats were randomly divided into normal control group,model control group,colchicine group,low-dose Kadsura coccinea group(2.5 g·kg^-1)and high-dose Kadsura coccinea group(5 g·kg^-1)(n=12).All groups except the normal control group were treated with CCl 4,rich fat and poor protein to establishexperimental hepatic fibrosis animal model.The second day after modeling,drug treatmentwas started,till the end of the sixth week.Pathological section of the rat’s liver was examined in order to observe its tissue under a optical microscope.Liver tissues were taken to examine the degree of liver fibrosis by HE and Masson staining,and the expression of Bcl-2,Bax and PCNA protein were detected by immunohistochemistry.Results Kadsura coccinea relieved the degree of necrosis of liver cells,liver fat’s degeneration and collagen fiber hyperplasia significantly.Compared with the model control group,expression of Bax in low-,high-dose Kadsura coccinea group and colchicine group were significantly decreased,and the expression of PCNA in hepatic fibrosis rats were enhanced(P<0.05 or P<0.01).Conclusion Kadsura coccinea has a certain inhibitory effects on experimental hepatic fibrosis in rats,and its mechanism may be related to inhibiting the expression of Bax protein and promoting the expression of PCNA protein in liver tissues.
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