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目的 观察脂多糖 (LPS)诱导肺泡巨噬细胞 (AM )p38蛋白激酶活化及抗炎药物地塞米松 (DEX)和N 乙酰半胱氨酸 (NAC)对其影响。方法 分离培养大鼠肺泡巨噬细胞 ,设正常对照组、LPS刺激组、DEX或NAC干预组 ,共 4组。分别采用Western印迹和放射免疫分析法检测AM核提取物 p38蛋白激酶和细胞培养上清TNF α、IL 8含量。 结果 LPS刺激组核蛋白提取物p38蛋白激酶和细胞培养上清TNF α、IL 8含量较正常对照组升高 (P <0 0 1 )。DEX组和NAC组虽较正常对照组高 ,但均低于LPS刺激组 (P <0 0 1 )。核提取物 p38蛋白激酶和细胞培养上清TNF α、IL 8含量之间分别呈正相关 (r =0 754、0 62 5 ,P <0 0 1 )。结论 LPS诱导肺泡巨噬细胞 p38蛋白激酶活化 ,进而导致TNF α、IL 8表达增多 ;DEX和NAC可能通过抑制 p38活化而减少炎性介质TNF α、IL 8的释放
Objective To investigate the effects of lipopolysaccharide (LPS) on the activation of p38 kinase in alveolar macrophages (AM) and the effects of anti-inflammatory drugs dexamethasone (DEX) and N-acetylcysteine (NAC). Methods Rat alveolar macrophages were isolated and cultured. The normal control group, LPS stimulation group, DEX or NAC intervention group were divided into 4 groups. Western blotting and radioimmunoassay were used to detect the levels of p38 protein kinase and TNFα and IL 8 in AM cell extracts. Results The levels of p38 protein kinase and cell supernatant TNFα and IL 8 in LPS stimulated group were higher than those in normal control group (P <0.01). Although the levels of DEX and NAC were higher than those of normal control group, they were lower than those of LPS stimulation group (P <0.01). Nuclear extracts of p38 protein kinase and cell culture supernatant TNFα, IL 8 content were positively correlated (r = 0 754,0 62 5, P <0 0 1). Conclusion LPS induces the activation of p38 protein kinase in alveolar macrophages, which leads to the increase of TNFα and IL-8 expression. DEX and NAC may reduce the release of TNFα and IL-8 by inhibiting the activation of p38