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Roles of nuclear factor-kappa B, tumor necrosis factor-α and Bcl-2 in acute hepatic injury and their mechanisms

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Author:
No author available
Journal Title:
WORLD CHINESE JOURNAL OF DIGESTOLOGY
Issue:
25
DOI:
10.3969/j.issn.1009-3079.2008.25.003
Key Word:
急性肝损伤;核因子-KB;肿瘤坏死因子-a;Bcl-2;免疫组化;放免法

Abstract´╝Ü 目的:探讨核因子-κB(nuelear factor-kappa B,NF-κB)及其下游因子TNF-α、Bcl-2在急性肝损伤的作用及机制.方法:(↑○) Wistar大鼠90只随机分为正常组,硫代乙酰胺(TAA)造模组及脯氨酸二硫代氨基甲酸酯(PDTC)预处理组(n=30).三组大鼠分别于造模完成后6、24、48 h 3个时间点处死.每个时间点各取10只大鼠.鲎试剂显色基质法测定大鼠血浆内毒素,放免法测定血浆TNF-α水平,取肝脏行病理学及免疫组化检测.制备肝脏单细胞悬液检测肝细胞凋亡指数.结果:与正常组相比,TAA细在6、24、48h时间点均可见血浆内毒素(Eu/mL)及TNF-α(ug/L)水平明显升高(内毒素:0.64±0.08 vs 0.23±0.02,P<0.01;0.96±0.14 vs 0.25±0.02,P<0.01;1.15±0.17 vs 0.25±0.03,P<0.01;TNF-α:5.97±1.07 vs 1.44±0.52,P<0.01;12.52±2.09 vs 1.57±0.62,P<0.01;10.76±1.95 vs 1.49±0.57.P<0.01),肝组织NF-κB及Bcl-2明显活化(NFκB:87.1l%±8.23% vs 4.64%±1.82%.78.55%±6.82% vs 4.58%±1.91%,74.27%±6.26%vs 4.73%±1.89%,均P<0.01;Bcl.2:51.11%±4.23% vs 6.74%±3.93%.71.59%±6.82% vs 6.68%±3.88%,82.19%±8.54% vs 6.81%±4.14%,均P<0.01).随着时间延长,肝细胞凋亡指数增加,TAA组肝脏病理变化明显,抑制NF-κB活性后,可见肝脏病理变化减轻.结论:TAA所致急性肝损伤中,TNF-α水平明显升高,发挥了促炎及诱导凋亡作用.其促凋亡作用相对拮抗Bcl-2抗凋亡作用.NF-κB通过调控其下游基因加重肝脏损伤.

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