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

59Citations
Citations of this article
50Readers
Mendeley users who have this article in their library.

Abstract

BACKGROUND: Activation 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. FINDINGS: In this study, we indicated that a novel natural anti-oxidant extracted from the Chinese plant Hopea 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 PPARgamma. CONCLUSIONS: MA has anti-inflammatory effects in MCAO mice in a PPARgamma-dependent manner, making it a potential candidate for stroke treatment.

Cite

CITATION STYLE

APA

Pan, J., Jin, J. li, Ge, H. ming, Yin, K. lin, Chen, X., Han, L. juan, … Xu, Y. (2015). Malibatol A regulates microglia M1/M2 polarization in experimental stroke in a PPARγ-dependent manner. Journal of Neuroinflammation, 12(1). https://doi.org/10.1186/s12974-015-0270-3

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free