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作 者:成秋宸[1] 赵永忠[1] 李胜联[1] 肖绪华[1] 刘瑞彪[1] 黄大健[1] 徐庆[1]
出 处:《医药论坛杂志》2013年第12期11-14,共4页Journal of Medical Forum
基 金:广西壮族自治区教育厅科研资助项目(201012MS172);广西壮族自治区自然科学基金项目(2012GXNSFAA053105)
摘 要:目的观察荔枝核总黄酮对胆汁淤积性肝纤维化大鼠肝功能指标的影响及对胶原蛋白的影响,探讨其可能的干预机制。方法将胆总管结扎后的SD大鼠分为胆总管结扎组(BDL组),荔枝核总黄酮组(TFL组),水飞蓟宾组(SIL组),以假手术组为阴性对照。四周后处死大鼠,取血清检测各组大鼠血清丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、直接胆红素(BILD2)、总胆红素(BILT2)、肌酐(CREJ2)、血尿素氮(UREAL),同时,取肝组织行HE、Masson染色,western blot测定各组肝组织的PC3、PCⅠ、p16的表达。结果与BDL组比较,TFL组血清SOD含量明显升高(P<0.05),ALT,AST,BILD2,BILT2水平明显降低(P<0.05),TFL可明显改善大鼠肝纤维化程度(P<0.05),且对肾功能无明显影响(P>0.05),TFL可明显抑制p16、PC3、PCⅠ蛋白的表达(P<0.05)。结论 TFL组(300mg/kg·d)有明显改善胆汁淤积及减轻肝组织纤维化的作用且对肾功能无明显影响,明显抑制胆汁淤积性肝纤维化大鼠肝脏p16、PC3、PCⅠ蛋白的表达,可能是通过诱导细胞凋亡途径抑制肝纤维化。Objective To investigate the function and mechanisim of total flavone from Litchi chinensis Sonn on collagen in eholestatic liver fibrosis rats. Methods The rats model of after ligation of the common bile duct into the common bile duct ligation( BDL group), Litchi flavonoids group( TFL group), silibinin group( SIL group), to the control group as a negative control. After four weeks, serum detection of serum alanine aminotransferase (ALT), aspartate aminotransferase ( AST), direct ilirubin ( BILD2), total bilirubin ( BILT2 ) , creatinine ( CREJ2 ), blood urea nitrogen (UREAL) were measured, and the pathological observation was also performed on legt liver lobes with HE, Masson staining, western blot were measured in liver tissue PC3, PC I , p16 expression. Results The serum SOD in TFL was significantly high er than that in the BDL group( P 〈 0.05 ), The serum ALT, AST, BILD2, BILT2 levels were significantly lower than that in the BDL group(P 〈0. 05 ), TFL can significantly improve the degree of hepatic fibrosis in rats(P 〈 0. 05), and no significant side effect on renal function ( P 〉 0. 05 ), TFL can inhibit p16, PC3, PC I protein expression ( P 〈 0. 05 ). Conclusions TFL group (300mg/kg.d) has a significant improvement in cholestasis and liver fibrosis mitigate and had no significant side effect on renal function, significantly inhibited cholestatic liver fibrosis in rat liver p16, PC3, PC I protein , probably by inducing apoptosis pathway inhibition of hepatic fibrosis.
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