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酒精性肝病(ALD)发病的重要机制在于饮酒导致肝巨噬细胞对内毒素——脂多糖(LPS)的敏感性升高,因而细胞内毒素(LPS)诱导信号相关机制在酒精肝损伤的初期和发展过程中发挥着至关重要作用。LPS被枯否细胞上的受体识别,激活下游信号通路,最终激活核转录因子(NF-κB),导致肿瘤坏死因子-α(TNF-α)、白细胞介素-1(IL-1)、白细胞介素-6(IL-6)和生长因子-β(TGF-β)等炎症细胞因子产生增加,炎症细胞因子又激活枯否细胞,产生更多细胞因子,加重肝脏损伤。
Alcoholic liver disease (ALD) pathogenesis is an important mechanism of drinking lead to liver macrophages increased endotoxin - lipopolysaccharide (LPS) sensitivity, and thus the mechanism of signal transduction induced by endotoxin (LPS) in alcoholic liver injury in the early And play a crucial role in the development process. LPS is recognized by receptors on Kupffer cells and activates downstream signaling pathway and ultimately activates nuclear factor-kappa B (NF-κB), leading to tumor necrosis factor-α (TNF-α), interleukin-1 Increased production of inflammatory cytokines, such as interleukin-6 (IL-6) and growth factor-β (TGF-β), activates Kupffer cells by inflammatory cytokines, producing more cytokines and aggravating liver damage.