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

Pan J, Jin JL, Ge HM, Yin KL, Chen X, Han LJ, Chen Y, Qian L, Li XX, Xu Y - J Neuroinflammation (2015)

Bottom Line: Microglia is reported with two opposing activated phenotypes, namely, classic phenotype (M1) and the alternative phenotype (M2).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).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.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Affiliated Drum Tower Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, China. panjie1000@hotmail.com.

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 PPARγ.

Conclusions: MA has anti-inflammatory effects in MCAO mice in a PPARγ-dependent manner, making it a potential candidate for stroke treatment.

No MeSH data available.


Related in: MedlinePlus

Effects of MA on inflammatory cytokines in LPS treated microglia. Q-PCR for mRNA expression of IL-6, iNOS, MCP-1, TNF-α, and IL-10 were shown. Values are mean ± SD. *P < 0.05 vs. con; #P < 0.05 vs. LPS; n = 6 in each group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
getmorefigures.php?uid=PMC4378556&req=5

Fig3: Effects of MA on inflammatory cytokines in LPS treated microglia. Q-PCR for mRNA expression of IL-6, iNOS, MCP-1, TNF-α, and IL-10 were shown. Values are mean ± SD. *P < 0.05 vs. con; #P < 0.05 vs. LPS; n = 6 in each group.

Mentions: The mRNA expression of IL-6, iNOS, MCP-1, and TNF-α were increased significantly after stimulated with LPS in primary microglia and reduced markedly at 15 h after treatment of MA. The expression of IL-10 in LPS-stimulated primary microglia showed significant increase after treatment with MA compared with non-treated group (Figure 3). These in vitro results are in accordance with the in vivo ones.Figure 3


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

Pan J, Jin JL, Ge HM, Yin KL, Chen X, Han LJ, Chen Y, Qian L, Li XX, Xu Y - J Neuroinflammation (2015)

Effects of MA on inflammatory cytokines in LPS treated microglia. Q-PCR for mRNA expression of IL-6, iNOS, MCP-1, TNF-α, and IL-10 were shown. Values are mean ± SD. *P < 0.05 vs. con; #P < 0.05 vs. LPS; n = 6 in each group.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4378556&req=5

Fig3: Effects of MA on inflammatory cytokines in LPS treated microglia. Q-PCR for mRNA expression of IL-6, iNOS, MCP-1, TNF-α, and IL-10 were shown. Values are mean ± SD. *P < 0.05 vs. con; #P < 0.05 vs. LPS; n = 6 in each group.
Mentions: The mRNA expression of IL-6, iNOS, MCP-1, and TNF-α were increased significantly after stimulated with LPS in primary microglia and reduced markedly at 15 h after treatment of MA. The expression of IL-10 in LPS-stimulated primary microglia showed significant increase after treatment with MA compared with non-treated group (Figure 3). These in vitro results are in accordance with the in vivo ones.Figure 3

Bottom Line: Microglia is reported with two opposing activated phenotypes, namely, classic phenotype (M1) and the alternative phenotype (M2).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).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.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, Affiliated Drum Tower Hospital of Nanjing University Medical School, 321 Zhongshan Road, Nanjing, 210008, China. panjie1000@hotmail.com.

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 PPARγ.

Conclusions: MA has anti-inflammatory effects in MCAO mice in a PPARγ-dependent manner, making it a potential candidate for stroke treatment.

No MeSH data available.


Related in: MedlinePlus