| 刘莉 刘锦程 仵倩红 牛国强 李伟 周祎.PPARγ对结核分枝杆菌脂蛋白P19诱导的巨噬细胞炎症反应的影响[J].,2014,14(22):4260-4264 |
| PPARγ对结核分枝杆菌脂蛋白P19诱导的巨噬细胞炎症反应的影响 |
| The Influence of PPARγ in Mycobacterium Tuberculosis LipoproteinP19-induced Inflammatory Response in Human Macrophages |
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| DOI： |
| 中文关键词: 结核分枝杆菌 19kDa 脂蛋白 PPARγ 巨噬细胞 炎症反应 |
| 英文关键词: Mycobcterium tuberulosis 19 kDa lipoprotein PPARγ Macrophage Inflammatory response |
| 基金项目:陕西省卫生厅科研基金项目《Toll 样受体及PPARr在结核分枝杆菌致病中的作用》 |
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| 中文摘要: |
| 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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