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Effect of mitogen-activated protein kinase pathway on Kupffer cell activation by lipopolysaccharide

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Author:
No author available
Journal Title:
CHINESE CRITICAL CARE MEDICINE
Issue:
8
DOI:
10.3760/j.issn:1003-0603.2002.08.004
Key Word:
丝裂原激活的蛋白激酶;脂多糖;肿瘤坏死因子;白介素;一氧化氮

Abstract: 目的:探讨丝裂素原激活蛋白激酶(MAPKs)途径在脂多糖(LPS)激活枯否细胞(KC)中的作用.方法:用3种MAPK通路阻滞剂,测定其后培养KC中肿瘤坏死因子α mRNA(TNF-α mRNA)、白介素-6 mRNA(IL-6 mRNA)以及诱生型一氧化氮合酶(iNOS)表达和TNF-α、IL-6以及NO的释放.结果:①ERK1/2途径抑制剂(PD098059)对KC中TNF-α mRNA表达和TNF-α的释放影响极小,而对IL-6 mRNA和iNOS的表达以及IL-6和NO的释放有明显的抑制作用;②p38MAPK途径抑制剂(SB203580)对KC中TNF-α mRNA和 IL-6 mRNA表达以及IL-6和TNF-α的释放影响极小,而对iNOS的表达和NO的释放有明显的抑制作用;③当用SB202474抑制整个MAPK途径时,KC中TNF-α、IL-6 mRNA和iNOS的表达和TNF-α、IL-6以及NO的释放均明显降低.结论:TNF-α mRNA表达和TNF-α的释放主要受MAPK途径中的JNK/SAPK途径的调节,IL-6 mRNA表达和IL-6的释放主要受MAPK途径中的ERK1/2和JNK/SAPK通路的调节,而iNOS的表达和NO的释放可能与以上3种途径均有关系.

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