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机构地区:[1]浙江大学附属第一医院ICU,杭州310003 [2]浙江大学附属邵逸夫医院麻醉科
出 处:《中华急诊医学杂志》2006年第4期328-330,共3页Chinese Journal of Emergency Medicine
摘 要: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 investigate modulatory effects of prostaglancdin E1 on the expressions of NF-kB and cytokines in serum, and to explore the protection mechanisms of PGE1 in ALI. Methods Forty-five male SD rats were randomly divided into three groups: group A (normal group, n = 15), group B (LPS group, n = 15) and group C (LPS + lipo-PGEl group, n = 15). The pathological changes and activity of NF-kB in the lung tissue, TNF-α, IL-10 and IL-12 concentration in serum at 1 hours, 2 hours and 4 hours after intraperitoneal LPS were observed. Results Hyperemia and edema of lung tissue in the LPS + lipo-PGE1 group was obviously less than that in the LPS group. Activity of NF-kB and serum concentrations of TNF-α and IL-12 in the LPS + lipo-PGE1 treated group were more decreased than that in the LtX3 group, and serum IL-10 concentration was obviously increased in the LPS + lipo-PGE1 group. Conclusion PGE1 reduced LPS-induced ALI through doun-regulating NF-kB activity and inhibiting expression of harmful inflammatory cytokines.
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