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目的观察不同机械牵张应力对大鼠肺泡巨噬细胞白介素-6(IL-6)和巨噬细胞炎症蛋白-2(MIP-2)的影响,并探讨C-JUN氨基末端激酶(JNK)对机械牵张诱导的大鼠肺泡巨噬细胞IL-6和MIP-2表达的调控作用。方法采用支气管肺泡灌洗的方法取得大鼠肺泡巨噬细胞,并建立体外大鼠肺泡巨噬细胞梯度应力的机械牵张模型,应用RT-PCR和Western印迹方法观察IL-6和MIP-2的表达。进一步应用JNK特异性抑制剂SP600125,p38特异性抑制剂SB203580,及ERK特异性抑制剂PD98059给予同期干预,检测干预效果。结果随着机械牵张应力的增大,肺泡巨噬细胞MIP-2 mRNA和其蛋白的表达递增(均P<0.05)。给予SP600125干预组大鼠肺泡巨噬细胞MIP-2 mRNA和蛋白表达较机械牵张处理组明显降低。SB203580干预组及PD98059干预组的肺泡巨噬细胞MIP-2 mRNA和蛋白水平较对照组明显升高,而与机械牵张处理组相比无明显变化。而IL-6 mRNA及其蛋白水平在上述各组中均无明显变化。结论大鼠巨噬细胞MIP-2的表达与机械牵张应力呈强度依赖性,JNK信号通路在周期性牵张诱导肺泡巨噬细胞表达释放MIP-2过程中起重要作用。
Objective To observe the effect of different mechanical distraction stress on interleukin-6 (IL-6) and macrophage inflammatory protein-2 (MIP-2) in rat alveolar macrophages, and to explore the effect of C-JNN-terminal kinase Regulation of IL-6 and MIP-2 expression induced by mechanical stretch in rat alveolar macrophages. Methods The alveolar macrophages were obtained by bronchoalveolar lavage (BAL) and mechanical stretch model of alveolar macrophage gradient stress in vitro was established. The expression of IL-6 and MIP-2 were observed by RT-PCR and Western blotting expression. The further application of JNK specific inhibitor SP600125, p38 specific inhibitor SB203580, and ERK specific inhibitor PD98059 given simultaneous intervention, the intervention effect. Results The expression of MIP-2 mRNA and its protein in alveolar macrophages increased with the increase of mechanical stretch stress (all P <0.05). The expression of MIP-2 mRNA and protein in alveolar macrophages in SP600125-treated group was significantly lower than that in mechanical stretch-treated group. Compared with the control group, MIP-2 mRNA and protein levels in alveolar macrophages of SB203580 intervention group and PD98059 intervention group were significantly increased, but no significant changes compared with mechanical stretch treatment group. The IL-6 mRNA and protein levels in the above groups did not change significantly. Conclusion The expression of MIP-2 in macrophages of rats is strongly dependent on mechanical stretch stress. JNK signaling pathway plays an important role in the cyclic stretch-induced expression of MIP-2 by alveolar macrophages.