摘要
非酒精性脂肪性肝病(nonalcoholic fatty liver disease,NAFLD)是代谢综合征的肝脏组分.代谢综合征代表慢性炎症状态,代谢综合征患者会呈现不同的免疫异常.脂肪组织的天然免疫功能紊乱导致机体产生异常的脂肪源性因子.某些因子抑制肝脏脂质清除,促进其在肝细胞内蓄积,产生脂肪变性.后者在肝脏先天性免疫系统发生Th-1极化的基础上诱导肝脏产生更多的致炎细胞因子,促进了非酒精性脂肪性肝炎(nonalcoholic steatohepatitis,NASH)的形成.但由于Th-2等其他细胞因子减少,尽管肝脏持续暴露于这些可以促进多种促纤维生成因子产生的致炎因子,NASH发展成肝硬化的现象却相对少见.
Nonalcoholic fatty liver disease (NAFLD) is the hepatic component of the metabolic syndrome. The metabolic syndrome represents a chronic inflammatory state, and individuals with the disorder demonstrate various immunologic abnormalities. Innate immune dysfunction in adipose tissue leads to abnormal production of adipose-derived factors, some of which can inhibit hepatic fat disposal and promote lipid accumulation within hepatocytes. The latter induces generation of excessive proinflammatory cytokines, particularly when the hepatic innate immune system becomes Th-1 polarized, thus promoting the development of nonalcoholic steatohepatitis (NASH). Although sustained exposure to these inflammatory mediators generally promotes the generation of various profibrogenic factors, progression from NASH to cirrhosis is actually relatively uncommon due to reduced production of other cytokines such as Th-2 cytokines.
出处
《世界华人消化杂志》
CAS
北大核心
2009年第30期3118-3122,共5页
World Chinese Journal of Digestology