OBJECTIVES: Our present study focused on assessing whether Sinomenine (SIN) could attenuate sepsis-induced acute lung injury (ALI). METHODS: The mice were conditioned with SIN 1 h before intraperitoneal injection of lipopolysaccharide (LPS). Lung wet/dry (W/D) ratio, inflammatory level in bronchoalveolar lavage fluid (BALF), malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity and inflammatory cytokines production were detected. The expression of nuclear factor erythroid 2-like 2 (Nrf2) and autophagy-related proteins were detected by Western blot and immunohistochemical analyses. In addition, the RAW264.7 cells were treated with SIN 1 h before treatment with LPS. Inflammatory cytokines, iNOS and COX2 were detected. The expression of Nrf2 and autophagy-related proteins were explored by Western blot analysis. KEY FINDINGS: Experiments in vivo and in vitro discovered that LPS significantly increased the degree of injury, inflammatory cytokines production and oxidative stress. However, the increase was significantly inhibited by treatment of SIN. In addition, SIN was found to upregulate the expression of Nrf2 and autophagy-related proteins both in vivo and in vitro. CONCLUSIONS: Our data suggested that SIN could attenuate septic-associated ALI effectively, probably due to the inhibition of inflammation and oxidative stress through Nrf2 and autophagy pathways.
OBJECTIVES: Our present study focused on assessing whether Sinomenine (SIN) could attenuate sepsis-induced acute lung injury (ALI). METHODS: The mice were conditioned with SIN 1 h before intraperitoneal injection of lipopolysaccharide (LPS). Lung wet/dry (W/D) ratio, inflammatory level in bronchoalveolar lavage fluid (BALF), malondialdehyde (MDA) levels, superoxide dismutase (SOD) activity and inflammatory cytokines production were detected. The expression of nuclear factor erythroid 2-like 2 (Nrf2) and autophagy-related proteins were detected by Western blot and immunohistochemical analyses. In addition, the RAW264.7 cells were treated with SIN 1 h before treatment with LPS. Inflammatory cytokines, iNOS and COX2 were detected. The expression of Nrf2 and autophagy-related proteins were explored by Western blot analysis. KEY FINDINGS: Experiments in vivo and in vitro discovered that LPS significantly increased the degree of injury, inflammatory cytokines production and oxidative stress. However, the increase was significantly inhibited by treatment of SIN. In addition, SIN was found to upregulate the expression of Nrf2 and autophagy-related proteins both in vivo and in vitro. CONCLUSIONS: Our data suggested that SIN could attenuate septic-associated ALI effectively, probably due to the inhibition of inflammation and oxidative stress through Nrf2 and autophagy pathways.