Salidroside Protects Lipopolysaccharide-Induced Acute Lung Injury in Mice

Salidroside (SDS) has been reported to have anti-inflammatory properties. The objective of this study was to investigate the protective effect of SDS on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice. BALB/c mice were pretreated with SDS 1 hour before intranasal instillation of LPS. Seven hours after LPS administration, the myeloperoxidase in histology of lungs, lung wet/dry ratio, and inflammatory cells in the bronchoalveolar lavage fluid (BALF) were determined. The levels of proinflammatory cytokines, tumor necrosis factor a (TNF-alpha), interleukin-1 beta (IL 1 beta), and IL-6 in the BALF were measured by enzyme-linked immunosorbent assay. The expression of Toll-like receptor 4 (TLR4), inhibitor of nuclear factor-kappa B (I kappa B-alpha), and nuclear factor-kappa B (NF-kappa B) p65 was detected by Western blot. The SDS reduced the inflammatory cells in BALF, decreased the wet/dry ratio of lungs, attenuated the LPS-induced histological alterations in the lung, and inhibited the production of TNF-alpha, IL-l beta, and IL-6. Western blot showed that SDS efficiently inhibited the phosphorylation of I kappa B-alpha, p65 NF-kappa B, and the expression of TLR4. These data show that the anti-inflammatory effects of SDS (at least 20 mg/kg) against LPS-induced ALI due to its ability to inhibit TLR4 mediated the NF-kappa B signaling pathways. The SDS may represent a novel strategy for treating LPS-induced ALI.