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作 者:张幸国[1] 虞朝辉[1] 蒋琦[1] 张宇[1] 陈韶华[1] 厉有名[1]
机构地区:[1]浙江大学医学院附属第一医院,浙江杭州310003
出 处:《中国中药杂志》2005年第11期847-850,共4页China Journal of Chinese Materia Medica
基 金:浙江省医药卫生科学研究基金项目(2003A036)
摘 要:目的:观察茶多酚抗大鼠酒精性肝损伤的细胞因子基因表达谱变化并探讨其作用机制。方法:大鼠随机分成3组,分别为酒精致模组(A组)、茶多酚治疗组(B组)和对照组(C组),在12周时观察各组肝脏标本组织损伤情况,并进行定量和半定量统计分析,同时用cDNA芯片测定肝脏组织的细胞因子表达水平。结果:与C组比较,A组和B组肝脏均出现不同程度的肝损伤表现。B组肝脏以脂肪变为主,其他肝损害较A组轻,表现在肝细胞肿胀程度较轻且面积较小,点、灶状坏死较少,未出现桥接坏死,脂变相对较轻,大泡性脂变相对较少,肝脏胶原沉积量少于A组。B组与A组比较:表达上调基因有IL-3,IL-4,IL-1R2,IL-6R,IL-7R2,表达下调基因有IL-3Ra,IL-1R1。A组与C组比较:表达上调基因有IL-13,IL-1R1,IL-7R2,EPO-R,LIFR,表达下调基因有IL-1R2,IL-5R2,CSF1,CD27,IL-6R。结论:茶多酚有抗大鼠酒精性肝损伤的作用,其作用机制可能与调节细胞因子的基因表达水平有关。Objective: To evaluate the effect of tea polyphenol(TP) on the rat with alcoholic liver damage. Method: Rats were divided into 3 groups, in which 2 groups were stomach perfused with alcohol to result in ALD, and 1 group of them stomach perfused with TP simultaneously. Another group was normal control groups(stomach perfused with dringking water). In the end of 12 weeks, the liver specimen of each rat was observed by anglicizing its tissue damage, and all data collected was performed by statistical analysis in quantum and semi-quantum. Meanwhile cytokines gene express of each group is determined. Result: In the end of 12 weeks, alcoholic hepatitis appeared in rat liver. Hepatic injury in alcohol group and TP group were found, but could not be found in normal group. Compared with pure alcohol group, alcoholic liver damage mainly showing with steatosis in TP group were slight, in addition showing liver cellular swelling with small area, with less spot and focal necrosis, none bridging necrosis. Steatosis were slight relatively, mega-bubble steatosis were less found. Collagen deposition of TP group were less than those of pure alcohol group. Gene expression of. cytokine have diversity statistically such as IL-3,IL-4,IL-1R2,IL-6R, IL-7R2, IL-3Ra,IL-1R1,IL-13,IL-1R1,IL-7R2,EPO-R,LIFR,IL-1R2,IL-5R2,CSF1,CD27,IL-6R. Conclusion: TP is able to attenuate alcoholic liver damage. It's mechanism is possibly due to modulating cytokines gene expression of cytokine.
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