Sangxingtang inhibits the inflammation of LPS-induced acute lung injury in mice by down-regulating the MAPK/NF-κB pathway

In the present study, we investigated anti-inflammatory effects of Sangxingtang(SXT) on acute lung injury using a lipopolysaccharide(LPS)-induced acute lung injury(ALI) mouse model. The cell counting in the bronchoalveolar lavage fluid(BALF) was performed. The degree of lung edema was evaluated by measuring the wet/dry weight(W/D) ratio. The superoxidase dismutase(SOD) and myeloperoxidase(MPO) activities were assayed by SOD and MPO kits, respectively. The levels of inflammatory mediators, including tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6), were assayed by the enzyme-linked immunosorbent assay methods. Pathological changes of lung tissues were observed by Hematoxylin and eosin(HE) staining. The inflammatory signaling pathway-related proteins nuclear factor mitogen activated protein kinases(P38MAPK), extracellular regulated protein kinases(Erk), c-Jun N-terminal kinase(Jnk) and nuclear transcription factor(NF-κB) p65 expressions were measured by Western blotting. Our results showed that the treatment with the SXT markedly attenuated the inflammatory cell numbers in the BALF, decreased the levels of P-P38 MAPK, P-Erk, P-Jnk and P-NF-κB p65 and the total protein levels in lungs, improved the SOD activity and inhibited the MPO activity. Histological studies demonstrated that SXT substantially reduced the LPS-induced neutrophils in lung tissues, compared with the untreated LPS group. In conclusion, our results indicated that SXT had protective effects on LPS-induced ALI in mice.