Protective effects of Rabdosia japonica var. glaucocalyx extract on lipopolysaccharide-induced acute lung injury in mice

The present study was designed to evaluate the protective effects of ethanol extracts of Rabdosia japonica var. glaucocalyx(Maxim.) Hara(RJ) on lipopolysaccharide(LPS)-induced acute lung injury(ALI) in mice and the possible underlying mechanisms of action. The mice were orally administrated with RJ extract(16, 32 or 64 mg?kg–1) daily for consecutive7 days before LPS challenge. The ung specimens and the bronchoalveolar lavage fluid(BALF) were collected for histopathological examinations and biochemical analyses. Pretreatment with RJ significantly enhanced superoxide dismutase(SOD) activity and reduced the wet-to-dry weight(W/D) ratio, the levels of nitric oxide(NO) and protein leakage, and myeloperoxidase(MPO) activity in mice with ALI, in a dose-dependent manner. RJ reduced complement deposition and significantly attenuated LPS-induced ALI by reducing productions of inflammatory mediators, such as tumor necrosis factor-α(TNF-α), interleukin-6(IL-6), and interleukin-1β(IL-1β). The results demonstrated that RJ may attenuate LPS-induced ALI via reducing the production of pro-inflammatory mediators, and reducing complement deposition and radicals.

The present study was designed to evaluate the protective effects of ethanol extracts of Rabdosia japonica var. glaucocalyx （Maxim.） Hara （RJ） on lipopolysaceharide （LPS）-induced acute lung injury （ALI） in mice and the possible underlying mechanisms of action. The mice were orally administrated with RJ extract （16, 32 or 64 mg.kg-1） daily for consecutive7 days before LPS challenge. The ung specimens and the bronchoalveolar lavage fluid （BALF） were collected for histopathological examinations and biochemical analyses. Pretreatment with RJ significantly enhanced superoxide dismutase （SOD） activity and reduced the wet-to-dry weight （W/D） ratio, the levels of nitric oxide （NO） and protein leakage, and myeloperoxidase （MPO） activity in mice with ALI, in a dose-dependent manner. RJ reduced complement deposition and significantly attenuated LPS-induced ALI by reducing productions of inflammatory mediators, such as tumor necrosis factor-a （TNF-a）, interleukin-6 （IL-6）, and interleukin-1β （IL-1β）. The results demonstrated that RJ may attenuate LPS-induced ALI via reducing the production of pro-inflammatory mediators, and reducing complement deposition and radicals.