Malibatol A regulates microglia M1/M2 polarization in experimental stroke in a PPARγ-dependent manner.

Malibatol A regulates microglia M1/M2 polarization in experimental stroke in a PPARγ-dependent manner.
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Malibatol A 以 PPARgamma 依赖性方式调节实验性中风中小胶质细胞 M1/M2 极化

DOI:
10.1186/s12974-015-0270-3
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发表时间:
2015-03-14
影响因子:
9.3
通讯作者:
Xu Y
Xu Y
中科院分区:
医学1区
文献类型:
--
作者:
Pan J;Jin JL;Ge HM;Yin KL;Chen X;Han LJ;Chen Y;Qian L;Li XX;Xu Y

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背景小胶质细胞的激活在缺血性中风后的免疫和炎症过程中起着至关重要的作用。据报道,小胶质细胞具有两种相反的激活表型,即经典表型 (M1) 和替代表型 (M2)。抑制M1同时刺激M2被认为是治疗中风的潜在治疗方法。在这项研究中,我们发现从中国植物海南希望草中提取的一种新型天然抗氧化剂马利巴醇A(MA)可以减少小鼠大脑中动脉闭塞(MCAO)后的梗塞面积并减轻脑损伤。 MA 不仅抑制 MCAO 小鼠的炎性细胞因子表达,还抑制脂多糖 (LPS) 刺激的小胶质细胞的表达。此外,MA治疗降低了M1标记物(CD16、CD32和CD86)并增加了M2标记物(CD206、YM-1),同时促进了核受体PPARγ的激活。结论MA以PPARγ依赖性方式在MCAO小鼠中具有抗炎作用,使其成为中风治疗的潜在候选者。
BackgroundActivation of microglia plays a crucial role in immune and inflammatory processes after ischemic stroke. Microglia is reported with two opposing activated phenotypes, namely, classic phenotype (M1) and the alternative phenotype (M2). Inhibiting M1 while stimulating M2 has been suggested as a potential therapeutic approach in the treatment of stroke.FindingsIn this study, we indicated that a novel natural anti-oxidant extracted from the Chinese plantHopea hainanensis, malibatol A (MA), decreased the infarct size and alleviated the brain injury after mice middle cerebral artery occlusion (MCAO). MA inhibited expression inflammatory cytokines in not only MCAO mice but also lipopolysaccharide (LPS)-stimulated microglia. Moreover, treatment of MA decreased M1 markers (CD16, CD32, and CD86) and increased M2 markers (CD206, YM-1) while promoting the activation of nuclear receptor PPARγ.ConclusionsMA has anti-inflammatory effects in MCAO mice in a PPARγ-dependent manner, making it a potential candidate for stroke treatment.
小胶质激活表型对阿尔茨海默氏病大脑中神经退行性和再生的分类。
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