Cryptotanshinone And Salidroside Prevent Lipopolysaccharide-induced Inflammation

Objective:To explore the mechanism of cryptotanshinone (CTN) and salidroside (SDS) against LPS-induced inflammation.Methods:RAW 264.7 cells were pretreated with various concentrations of CTN or SDS for 1 h and then stimulated with 1μg/ml LPS for 30 min or 24 h.Results:LPS significantly increased the levels of NO, phosphorylated TAK and the expression of iNOS, COX-2. CTN inhibited the production of NO production, as well as expression of iNOS, COX-2 in LPS-stimulated macrophages, reduced the expression of CD 14, TLR4, and suppressed LPS-induced phosphorylation of TAKl.LPS also increased the expression of NF-κB protein and phosphorylated MAPKs. Pretreatment with non-toxic concerntrations of SDS inhibited iNOS, COX-2, CD 14, TLR4 and p-TAK at protein expression. SDS also inhibited nuclear translocation of NF-κB and MAPK phosphorylation.Conclusion:CTN inhibited LPS-induced proinflammatory mediators via TLR4 and TAKl signaling pathway. High dose of CTN (40 mg/kg) can significantly inhibit the increase the indices of spleen and liver. In vivo experiments showed that CTN has anti-inflammatory effect.SDS inhibited LPS-induced proinflammatory mediators via NF-κB and MAPKs signaling pathway. SDS (100 mg/kg) can significantly inhibit the increase the indices of spleen and lung. In vivo experiments showed that SDS has anti-inflammatory effect.