Enhanced inflammatory response and oxidative stress cause acute lung injury(ALI). Controlling inflammation and oxidation can ameliorate ALI. In the present study, we aimed to determine whether 3,4-Dihydroxyacetophenon...Enhanced inflammatory response and oxidative stress cause acute lung injury(ALI). Controlling inflammation and oxidation can ameliorate ALI. In the present study, we aimed to determine whether 3,4-Dihydroxyacetophenone(compound 1)could ameliorate lipopolysaccharide(LPS)-induced ALI by suppressing inflammation and oxidation. In this study, compound 1 reduced LPS-induced inflammatory cytokines and oxidative stress in RAW 264.7 cells. Moreover, compound 1 suppressed the expression of inflammatory protein p65, inhibited IkBα phosphorylation, decreased the nuclear translocation of p65, and increased the expressions of anti-oxidative protein nuclear factor erythroid 2-related factor 2(Nrf-2) and heme oxygenase-1(HO-1), which was reduced by LPS, in leukemia cells in mouse macrophage(RAW 264.7) cells. Furthermore, compound 1 could also ameliorate LPS-induced ALI in vivo, with a reduction of inflammatory cytokines, oxidative stress, and nuclear factor-kappa B(NF-κB)signaling pathway activation. This study emphasized the anti-inflammatory and anti-oxidative activities of compound 1, which could be a valuable therapeutic agent against ALI.展开更多
基金National Natural Science Foundation of China (Grant No. 82003755)the Medical Technology Program of Ningbo (Grant No. 2019Y07)。
文摘Enhanced inflammatory response and oxidative stress cause acute lung injury(ALI). Controlling inflammation and oxidation can ameliorate ALI. In the present study, we aimed to determine whether 3,4-Dihydroxyacetophenone(compound 1)could ameliorate lipopolysaccharide(LPS)-induced ALI by suppressing inflammation and oxidation. In this study, compound 1 reduced LPS-induced inflammatory cytokines and oxidative stress in RAW 264.7 cells. Moreover, compound 1 suppressed the expression of inflammatory protein p65, inhibited IkBα phosphorylation, decreased the nuclear translocation of p65, and increased the expressions of anti-oxidative protein nuclear factor erythroid 2-related factor 2(Nrf-2) and heme oxygenase-1(HO-1), which was reduced by LPS, in leukemia cells in mouse macrophage(RAW 264.7) cells. Furthermore, compound 1 could also ameliorate LPS-induced ALI in vivo, with a reduction of inflammatory cytokines, oxidative stress, and nuclear factor-kappa B(NF-κB)signaling pathway activation. This study emphasized the anti-inflammatory and anti-oxidative activities of compound 1, which could be a valuable therapeutic agent against ALI.
