论文部分内容阅读
Alcoholic liver disease (ALD) is associated with a spectrum of liver injury ranging from steatosis and steatohepatitis to fibrosis and cirrhosis.In response to gut-derived lipopolysaccharide (LPS), activation of Kupffer cells plays a key role in the development and progression of ALD by secreting a variety of pro-inflammatory cytokines.Consequently, inhibition of macrophage-activation would have therapeutic benefits for alleviating the progression of ALD.Salidroside (Sal), one of main bioactive components isolated from Rhodiola Sachalinensis, has been reported to suppress LPS-induced inflammatory response, but the underlying mechanisms in macrophages remain poorly understood.In this study, we investigate the anti-inflammatory effects of Salidroside and the possible mechanisms in LPS-stimulated phrobol 12-myristate 13-acetate (PMA)-differentiated THP-1 macrophage models.The results showed that Sal markedly decreased the expression of inducible nitric oxide synthase (iNOS), cyclooxygenase-2(COX2), interleukin-lbeta (IL-1β), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) at both mRNA and protein levels, and there was dose-effect relationship between the three Sal pretreated groups.Further studies revealed that Sal strongly suppressed NF-κB activation and down-regulated the phosphorylation of ERK,p38 and JNK.Our present study demonstrated that Sal could suppress the production of iNOS, COX2, IL-1β, IL-6 and TNF-α in LPS-stimulated PMA-differetiated THP-1 cells by inhibiting NF-rB activation and MAPK signal pathway phosphorylation.