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目的：探讨PPARγ对结核分枝杆菌细胞壁成分19 kDa 脂蛋白(M.tb-P19)诱导的巨噬细胞免疫反应的影响。方法：以 M.tbH37Rv 和M.tb-P19 刺激人源性巨噬细胞48 h，观察其对巨噬细胞PPARγ表达的影响。分别采用激动剂、拮抗剂干预PPARγ活性，观察PPARγ被激活或抑制后对M.tb-P19 诱导的ERK磷酸化、NF-ΚB 的表达以及炎症细胞因子IL-6、TNF-α的表达的影响。结果：M.tb -P19 感染的人巨噬细胞中PPARγ的表达较正常对照细胞显著升高，且随作用时间的延长逐渐增加(P<0.05)，48h 达高峰。M.tb-P19 感染可显著增加人巨噬细胞中磷酸化ERK、NF-κB、TNF-α和IL-6 的表达(P<0.05)，PPAR酌激动剂预处理可显著抑制M.tb-P19 感染所致的磷酸化ERK、NF-κB、TNF-α和IL-6 的表达增加(P<0.05)，而PPARγ拮抗剂预处理可进一步提高磷酸化 ERK、NF-κB、TNF-α和IL-6 的表达(P<0.05)。结论：PPAR酌可能是通过激活ERK及NF-κB 信号通路，抑制M.tb-P19 所介导的巨噬细胞炎症反应。

英文摘要:

Objective:To investigate the effect of PPARγon Mycobacterium tuberculosis lipoprotein P19 (M.tb -P19)-induced inflammatory response in human macrophages.Methods:M.tb H37Rv and M.tb-P19 were used to stimulate human macrophages for 48 h. Its effect on macrophage PPARγexpression were observed. By using the agonist/antagonist of PPARγ, the effect of PPARγactivation or inhibition on M.tb-P19-induced phosphorylation of ERK, NF-kB and the expression of inflammatory cytokines such as IL-6, TNF-α expression were investigated.Results:Human macrophages infected with M.tb-P19 for 12 h induced the increase of PPARγ expression with the extended response time (P<0.05), which reached the peak at 48h. Infection with M.tb-P19 could significantly increase the phosphorylation of ERK, NF-kB, TNF-αand IL-6 expression (P<0.05). Furthermore, PPARγagonists could significanly block the phosphorylation of ERK, NF-kB, TNF-αand IL-6 expression (P<0.05), while PPARγ antagonist could significantly increase the phosphorylation of ERK, NF-kB, TNF-αand IL-6 expression(P<0.05).Conclusion:PPARγmay inhibite M.tb-P19 induced inflammatory responses in human macrophages through activating the ERK and NF-kB signaling pathways

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