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目的探讨脂氧素A4对脂多糖诱导小鼠急性肺损伤的影响。方法36只雄性C57BL/6小鼠,随机分为对照组、脂氧素A4组、ZnPP组、内毒素组、脂氧素A4治疗组(LXA4+LPS)和ZnPP+脂氧素A4治疗组(ZnPP+LXA4+LPS),每组6只。雾化吸入脂多糖8h后,测定肺泡灌洗液白细胞计数、中性粒细胞计数和TNF-α含量。测定肺组织髓过氧化物酶(MPO)活性、HO-1的蛋白表达和活性。结果与LPS组比较,脂氧素A4治疗组肺组织中性粒细胞浸润减少,MPO活性、TNF-α浓度均降低(P<0·01),肺组织损伤减轻,而HO-1的蛋白表达和活性明显升高,HO-1抑制剂ZnPP减弱脂氧素A4的保护作用。结论脂氧素A4能减轻内毒素诱导的急性肺损伤。
Objective To investigate the effect of lipoxin A4 on lipopolysaccharide-induced acute lung injury in mice. Methods 36 male C57BL / 6 mice were randomly divided into control group, lipoxin A4 group, ZnPP group, endotoxin group, LXA4 + LPS group and ZnPP + lipoxin A4 group + LXA4 + LPS), 6 in each group. After 8h inhalation of lipopolysaccharide, the leucocyte count, neutrophil count and TNF-αlevel of BALF were measured. Pulmonary myeloperoxidase (MPO) activity, HO-1 protein expression and activity were determined. Results Compared with the LPS group, the neutrophil infiltration, the MPO activity and the concentration of TNF-α in the lung tissue of the lipoxygenin-A4 treated group were decreased (P <0.01) and the lung tissue lessened, while the protein expression of HO-1 And activity was significantly increased, HO-1 inhibitor ZnPP weakened the protective effect of lipoxin A4. Conclusion Lipoxin A4 can attenuate endotoxin-induced acute lung injury.