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机构地区:[1]咸宁学院附属第一医院内科,湖北咸宁437100 [2]华中科技大学同济医学院附属同济医院内科
出 处:《咸宁学院学报(医学版)》2006年第1期11-13,17,共4页Journal of Xianning Univarsity(medical Sciences)
摘 要:目的探讨p38蛋白激酶在脂多糖(LPS)刺激肺泡巨噬细胞激活机制中的作用。方法分离培养大鼠肺泡巨噬细胞,设正常对照组、LPS刺激组、SB203580干预组(SB203580+LPS组)。分别采用免疫组织化学和原位分子杂交方法检测p38蛋白质及其mRNA的表达,用放射免疫分析法检测细胞培养上清TNF-αI、L-8的含量。结果LPS刺激肺泡巨噬细胞p38胞核染色阳性细胞百分比、胞浆p38mRNA的表达以及培养上清TNF-αI、L-8含量显著升高,分别为正常对照组的5.75倍、1.44倍、3.57倍和3.22倍;加入SB203580预处理后,上述指标均较LPS刺激组显著下降,较正常对照组稍高,但差异无显著性。肺泡巨噬细胞p38蛋白质胞核染色阳性细胞百分比及其mRNA的表达与培养上清TNF-αI、L-8含量均呈显著正相关。结论LPS刺激肺泡巨噬细胞释放炎性细胞因子可能是通过p38蛋白激酶介导的,抑制p38的活性可能成为治疗炎症反应的一条新途径。Objective To investigate the role of p38 protein kinase in the activation of alveolar macrophages(AMs) induced by lipopolysaccharide(LPS). Methods AMs isolated and purified from normal rats which were divided into three groups: control group, LPS-stimulated group and SB203580+ LPS group. The expression of p38 protein and mRNA were observed by immunocytochemical staining and in situ hybridization staining respectively. The concentrations of TNF-α and IL-β in supernatants were measured by radioimmunoassay. Results The percentages of positive cells of p38 protein, p38 mRNA and the levels of TNF-αand IL-β in LPS-stimulated group were significantly higher than those in control group(P〈0. 01). By using SB203580 before LPS stimulated, the above indexes were significantly reduced compared with those in LPS-stimulated group(P〈0. 01), and still higher but not significantly compared with those in control group(P〈0.05). There were good positive correlation between the percentage of positive cells of p38 protein, p38 mRNA and the concentrations of TNF-α and IL-β in supernatant (r=0.751,0. 635,0. 712 and 0. 845, P〈0. 01). Conclusion These results indicate that p38 protein kinase plays an important role in the LPS-activated signaling pathway that regulates TNF-α and IL-β production by AMs. Inhibiting the activity of p38 protein kinase may be useful to treat the inflammatory diseases.
关 键 词:脂多糖 肺泡巨噬细胞p38蛋白激酶 肿瘤坏死因子-α 白细胞介素-Β
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