TLR4信号传导通路与胰腺炎

Toll-like receptor 4 signaling pathway and pancreatitis

胰腺炎的发病机制长期以来一直是基础和临床研究的一个重要课题,然而至今尚不完全明确.研究证实TLRs(Toll-like receptors)家族成员中TLR4可与G-菌内毒素脂多糖(lipopolysaccharide,LPS)结合,通过NF-κB信号通路激发多种炎症因子的合成进而参与多种器官疾病的发病过程.在鼠类模型和临床研究中已经显示TLR4信号通路在急性胰腺炎(acute pancreatitis,AP)的发病过程中起着重要的作用;上调TLR4信号通路可诱导致炎细胞因子大量释放参与重症急性胰腺炎(severe acute pancreatitis,SAP)病程中多器官功能障碍综合征的形成.因此,进一步明确TLR4信号通路在胰腺炎发病机制的作用,有可能通过阻断TLR4信号通路使胰腺炎获得疗效.

The pathogenesis of pancreatitis has long been a hot topic in basic and clinical research but is still not fully clarified.Toll-like receptor 4（TLR4） recognizes the lipopolysaccharide（LPS） of Gram-negative bacteria and stimulates the synthesis and release of inflammatory cytokines through activation of the NF-κB signaling pathway,which ultimately results in inflammatory responses that involve multiple organs.Animal and clinical studies have shown that the TLR4 signal pathway plays an important role in the development of tissue injury during acute pancreatitis（AP） and up-regulation of TLR4 and the TLR4 signaling pathway contributes to the development of multiple organ dysfunction syndrome（MODS） associated with severe acute pancreatitis（SAP） by increasing proinflammatory cytokines.Therefore,further studies are required to clarify the role of the TLR 4 signaling pathway in the pathogenesis of pancreatitis to explore novel methods for treating this disease.