Modulation of tumor necrosis factor-alpha and oxidative stress through protein kinase C and P42/44 mitogen-activated protein kinase in lead increases lipopolysaccharide-induced liver damage in rats

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 健康照護學院 > 物理治療學系暨復健科學碩士班 > 期刊論文 > Item 310903500/28448

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題名:	Modulation of tumor necrosis factor-alpha and oxidative stress through protein kinase C and P42/44 mitogen-activated protein kinase in lead increases lipopolysaccharide-induced liver damage in rats
作者:	鄭宇容(Cheng, Yu-Jung);劉明毅(Liu MY)*
貢獻者:	健康照護學院物理治療學系
關鍵詞:	Lipid peroxidation;nitric oxide;protein kinase C;p42/44 mitogen-activated protein kinase;tumor necrosis factor-[alpha]
日期:	2005-08
上傳時間:	2010-09-23 19:55:44 (UTC+8)
摘要:	Lead (Pb) increases lipopolysaccharide (LPS)-induced tumor necrosis factor-alpha (TNF-alpha), nitric oxide (NO), lipid peroxidation (LPO), and liver damage. In this study, we investigated the role of protein kinase C (PKC) and p42/44 mitogen-activated protein kinase (MAPK) and the causal relationships between TNF-alpha, NO, and LPO in Pb-increased LPS-induced liver damage in rats. Treatment with PKC and p42/44 MAPK inhibitors significantly reduced Pb + LPS-induced NO, TNF-alpha, LPO, and liver damage, which was revealed by elevated serum levels of aspartate aminotransferase and alanine aminotransferase. Pb + LPS coexposure significantly increased phosphorylation of p42/44 MAPK and TNF-alpha expression in peripheral blood cells; however, exposure to Pb + LPS did not induce TNF-alpha, NO, or LPO production and p42/44 MAPK activation in the liver. Pentoxifylline, a TNF-alpha inhibitor, also reduced liver damage but did not alter NO or LPO in Pb + LPS-treated rats. Thus, Pb increased LPS-induced liver damage through PKC and p42/44 MAPK modulation of TNF-alpha and oxidative stress, but modulation of TNF-alpha did not affect NO or LPO in rats.
關聯:	SHOCK 24(2):188-193
顯示於類別:	[物理治療學系暨復健科學碩士班] 期刊論文

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