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目的建立急性肺损伤(ALI)大鼠模型,通过观察脂微球前列腺素E1(1ipoPGEl)对肺组织核因子-κB(NF-κB)活化的调控作用和对血清中细胞因子表达的调控作用,探讨PGE1对ALI的保护作用机制。方法雄性SD健康大鼠45只随机分成3组,A组:生理盐水组;B组:LPS模型组;C组:LPS+lipoPGE1治疗组。各组分1、2、4h3个时间点各5只观察肺组织变化,测定肺组织NF-κB的表达及血清细胞因子TNFα、IL-12、IL-10浓度。结果治疗组肺组织充血出血情况较模型组明显改善,NF-κB表达显著降低,血清TNF-α、IL-12浓度显著降低,IL-10浓度明显增高。结论前列腺素E1通过下调NFκB的活性,抑制炎症因子的表达从而减轻急性肺损伤。
Objective To establish a rat model of acute lung injury (ALI) by observing the regulation of nuclear factor-κB (NF-κB) activation and the regulation of cytokines expression in serum by lipopolynaphyroid prostaglandin E1 (1ipoPGE1) To explore the protective mechanism of PGE1 on ALI. Methods Forty-five male SD rats were randomly divided into three groups: group A: saline group; group B: LPS model group; group C: LPS + lipoPGE1 treatment group. At 1, 2 and 4 hours after operation, the changes of lung tissue were observed in 5 of 3 time points. The expression of NF-κB and the levels of TNFα, IL-12 and IL-10 in serum were measured. Results The hyperemia and hemorrhage of lung tissue in the treatment group was significantly improved compared with the model group, the expression of NF-κB was significantly decreased, the concentration of serum TNF-α and IL-12 was significantly decreased and the concentration of IL-10 was significantly increased. Conclusions Prostaglandin E1 attenuates acute lung injury by down-regulating the activity of NFκB and inhibiting the expression of inflammatory cytokines.