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作 者:王凤林[1] 杨宏志[1] 李杨湄[1] 吴伟康[1,2] 邹增城
机构地区:[1]中山大学附属第三医院中医科,广东广州510630 [2]中山大学中西结合研究所,广东广州510080
出 处:《中药材》2014年第5期848-852,共5页Journal of Chinese Medicinal Materials
摘 要:目的:探讨以茵陈蒿汤联合大承气汤为基础的清下法对急性内毒素肝损伤大鼠肝细胞凋亡防治作用。方法:采用内毒素(LPS)加D-氨基半乳糖(D-GalN)造成大鼠急性内毒素性肝损伤模型,并予以清下中药进行干预,检测造模后各组大鼠肝功能及凝血酶原时间、肝组织病理改变,Tunel检测各组大鼠肝细胞凋亡指数,Western-blot检测各组大鼠肝组织BCL-2、BAX及Caspase-3蛋白表达量。结果:与模型组比较,清下法可显著降低内毒素性肝损伤大鼠血ALT、AST、TBIL水平(P<0.05或P<0.01),减轻肝细胞的坏死及炎性细胞浸润。Tunel检测显示模型组可见较多凋亡细胞,与对照组及清下组相比均有显著差异(P<0.01),模型组大鼠BAX、Caspase-3蛋白表达量显著高于对照组及清下组(P<0.05),BCL-2蛋白表达量则较对照组及清下组显著降低(P<0.05)。结论:清下法可显著改善内毒素性肝损伤大鼠肝功能及肝组织病理、降低肝细胞凋亡率,其机制可能是通过降低BAX、Caspase-3蛋白表达,上调BCL-2蛋白表达,调节BCL-2/BAX之间的平衡而起到防治内毒素所致肝细胞凋亡的作用。Objective:To study the prevention and treatment mechanism of Qingxia therapy( based on Yinchenhao Decoction and Dachengqi Decoction) on hepatocyte apoptosis in rats with acute hepatic injury induced by lipopolysaccharide plus D-galactosamine (LPS/D-GalN). Methods:The acute hepatic injury model was established by LPS/D-GalN and then intervened with Qingxia therapy. Serum liver function, PT and liver tissue pathology were observed, hepatocyte apoptosis index was detected by Tunel, protein expreso sions of BCL-2, BAX and Caspase-3 were detected by Western blotting. Results : Qingxia therapy could significantly decrease serum ALT, AST and TBIL levels (P 〈 O. 01 or 0. 05 ) , reduce hepatocyte necrosis and inflammatory cell infiltration. There were more apoptotie cells in model group ,which had significant differences compared with Qingxia group and control group. Protein expressions of BAX and Caspase-3 in model group were significantly higher than those in control group and Qingxia group( P 〈 0.05 ), but BCL-2 protein expres- sion in model group was lower( P 〈 0.05 ). Conclusion : Qingxia therapy can ameliorate the liver function and hepatic tissue pathology of rats with hepatic injury induced by LPS/D-GalN, alleviate hepatocyte apoptosis in rats, prevent and treat hepatocyte apoptosis by down- regulating the protein expressions of Caspase-3 and BAX, up-regulating the protein expression of BCL-2, and adjusting the balance of BCL-2/BAX.
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