摘要
肝衰竭是多种病因引起的肝功能失代偿,其发病机制涉及肝细胞的坏死、凋亡、再生、肝脏纤维化等。Toll样受体(TLR)作为一种模式识别受体,参与了固有免疫反应和获得性免疫反应,在肝衰竭的发病中起重要作用。动物实验和临床研究均已证实TLR与肝细胞的坏死有关。脂多糖(LPS)、D-氨基半乳糖(D-GalN)、刀豆素A(ConA)、CpG寡脱氧核苷酸(CpG ODN)、多聚肌苷酸-多聚胞苷酸(Poly I:C)和对乙酰氨基酚(APAP)所致的肝损伤需要不同的TLR通路参与。TLR3、TLR4、TLR9参与了肝细胞的凋亡。TLR7对肝纤维化有保护作用。TLR基因多态性研究可以从宿主方面揭示肝衰竭的发病机制,为个体化诊疗提供依据。
Liver failure caused by many etiologies,is a deficiency of liver. Its pathogenesis still remains unclear,and it might involve necrosis,apoptosis and regeneration of the hepatocytes,and fibrosis of the liver. As a kind of pattern recognition receptor,Toll-like receptors （TLRs） link the innate and adaptive immune response,and play an important role in the pathogenesis of liver failure. Animal experiments and clinical studies have demonstrated that TLRs are related to the necrosis of liver cells. Liver injury which is caused by different agents,such as LPS,D-GalN,ConA,CpG ONA,Poly （I：C）and APAP,needs different TLRs signaling. TLR3,TLR4 and TLR9 signaling can promote apoptosis of liver cells. TLR7 signaling has a protective effect against liver fibrosis. Research on TLR polymorphism can reveal the pathogenesis of liver failure from the host aspect , and provide evidences for individualized diagnosis and treatment of patients with liver failure.
出处
《实用肝脏病杂志》
CAS
2014年第6期665-668,共4页
Journal of Practical Hepatology
基金
国家973项目十二五重大科技专项(2012ZX10002007)
关键词
肝衰竭
TOLL样受体
凋亡
Liver failure
Toll like receptor
Apoptosis
