【摘要】 目的探讨Maresin-1(MaR1)治疗脂多糖(LPS)诱导的急性肺损伤(ALI)小鼠的效果和机制。方法将雄性SPF级BALB/c小鼠45只随机分为3组。对照组经口气管插管滴入3 mg/kg生理盐水。LPS组经口气管插管滴入3 mg/kg LPS。MaR1组经口气管插管滴入3 mg/kg LPS,1 h后尾静脉注射1 ng/只MaR1。对比分析3组小鼠肺组织损伤评分、免疫印迹分析小鼠肺组织MAPKs、核因子-κB(NF-κB)蛋白表达,以及氧化应激标记分析3组小鼠肺组织核因子-E2相关因子2(Nrf-2)表达和抗氧化酶的情况。结果与LPS组比较,MaR1组能改善LPS诱导的ALI小鼠肺组织损伤评分(P=0.000);MaR1组能显著抑制LPS诱导的ALI小鼠MAPKs和p65NF-κB的磷酸化,两组间差异均有统计学意义(P<0.05);MaR1组通过上调抗氧化酶增加Nrf-2的核转运,两组间差异均有统计学意义(P<0.05);MaR1组抑制了LPS诱导的ALI模型肺组织中活性氧介导的氧化应激反应,两组间差异均有统计学意义(P<0.05)。结论 MaR1治疗小鼠ALI机制可能是通过抑制MAPK和NF-κB的磷酸化,同时活化多种抗氧化酶保护肺组织有关。更多还原

【Abstract】 Objective To investigate the effect and mechanism of maresin-1(MaR1) on lipopolysaccharide-induced acute lung injury(ALI) in mice.Methods Forty-five male SPF BALB/c mice were randomly divided into 3 groups, control group(3 mg/kg normal saline was injected via endotracheal intubation), LPS group(3 mg/kg LPS via endotracheal intubation), and MaR1 group(3 mg/kg LPS via endotracheal intubation via endotracheal intubation). The expression of MAPKs, NF-κB, nuclear factor E2-related factor 2(nrf-2) and antioxidant enzymes in the lung tissues of mice were compared. Results Compared with LPS group, MaR1 group significantly improved lung tissue injury score of ALI mice induced by LPS(P=0.000). The phosphorylation of MAPKs and p65 NF-κB in ALI mice induced by LPS was significantly inhibited in the MaR1 group(P<0.05). The nuclear transport of Nrf-2 was significantly increased by upregulation of antioxidant enzymes in the MaR1 group(P<0.05). The MaR1 group significantly inhibited the oxidative stress response mediated by reactive oxygen species in the lung tissue of LPS-induced ALI model(P<0.05). Conclusion The mechanism of MaR1 in the treatment of ALI in mice may be related to the protection of lung tissue by inhibiting the phosphorylation of MAPK and NF-κB, and activating various antioxidant enzymes.更多还原