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首页> 外文期刊>Biochemical and Biophysical Research Communications >Curcumin inhibits 19-kDa lipoprotein of Mycobacterium tuberculosis induced macrophage apoptosis via regulation of the JNK pathway
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Curcumin inhibits 19-kDa lipoprotein of Mycobacterium tuberculosis induced macrophage apoptosis via regulation of the JNK pathway

机译：姜黄素通过调节JNK途径抑制结核分枝杆菌诱导的巨噬细胞凋亡的19-kDa脂蛋白

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摘要

Recently, synthetic curcumin analogs are reported as potential active compounds against Mycobacterium tuberculosis (MTB). During the process of MTB infection, macrophages show increased apoptosis. The candidate virulence factors such as 19-kDa lipoprotein secreted by the MTB (P19) strongly influences macrophages by activation of Toll-like receptor 2 (TLR2) and mitogen-activated protein kinases (MAPKs). It has been reported that curcumin could affect the apoptosis of tumor cells via regulation of MAPKs. However, its effect on the P19-induced apoptosis of macrophages is unclear. This study investigates the effect of curcumin on the MAPKs signaling and apoptosis in human macrophages. The results showed that curcumin and P19 induced macrophage apoptosis in a time- and dose-dependent manner Low doses of curcumin (10 and 20 μM) protected macrophages from P19 induced apoptosis, accompanied by decreased production of cytokines and reduced activation of the c-Jun amino-terminal kinase (JNK) and p38 MAPK. The protective effect of curcumin on P19 induced apoptosis of macrophages were enhanced by treatment with the JNK-specific inhibitors, whereas SB203580, the inhibitor of p38 MAPK had no effect. Curcumin had no effect on the activity of extracellular signal-regulated protein kinase (ERK). Taken together, our data show that the JNK pathway, but not the p38 or ERK pathway, plays an important role in the protective effect of curcumin against P19 induced macrophage apoptosis, and regulation of the JNK pathway may partially elucidate the anti-tuberculosis activity of curcumin.
机译：最近，据报道合成姜黄素类似物是抗结核分枝杆菌（MTB）的潜在活性化合物。在MTB感染过程中，巨噬细胞显示出凋亡增加。候选毒力因子（例如由MTB分泌的19 kDa脂蛋白（P19））通过激活Toll样受体2（TLR2）和促分裂原激活的蛋白激酶（MAPK）强烈影响巨噬细胞。已有报道姜黄素可通过调节MAPKs影响肿瘤细胞的凋亡。但是，其对P19诱导的巨噬细胞凋亡的影响尚不清楚。这项研究调查姜黄素对人类巨噬细胞MAPKs信号转导和凋亡的影响。结果表明，姜黄素和P19以时间和剂量依赖性方式诱导巨噬细胞凋亡。低剂量的姜黄素（10和20μM）可以保护巨噬细胞免于P19诱导的细胞凋亡，并伴随细胞因子生成减少和c-Jun激活降低氨基末端激酶（JNK）和p38 MAPK。姜黄素通过JNK特异性抑制剂的作用增强了P19诱导的巨噬细胞凋亡的保护作用，而p38 MAPK抑制剂SB203580没有作用。姜黄素对细胞外信号调节蛋白激酶（ERK）的活性没有影响。综上所述，我们的数据表明，JNK途径而不是p38或ERK途径在姜黄素对P19诱导的巨噬细胞凋亡的保护作用中起着重要作用，而JNK途径的调节可能部分阐明了姜黄素的抗结核活性。姜黄素。

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