Carcinogenesis, Teratogenesis & Mutagenesis ›› 2018, Vol. 30 ›› Issue (2): 98-102.doi: 10.3969/j.issn.1004-616x.2018.02.004

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Mechanism of proanthocyanidin-mediated inhibition of LPS-induced activation of microglial cells

ZHANG Yan1,2, ZHANG Xiaoqiang1,2, LIANG Xiaoyu1,2, WANG Xu1,2, LIU Jing1,2   

  1. 1. School of Public Health, Southeast University, Nanjing 210009;
    2. Key Laboratory of Environmental Medicine, Engineering of Ministry of Education, Southeast University, Nanjing 210009, Jiangsu, China
  • Received:2017-11-23 Revised:2018-03-02 Online:2018-03-30 Published:2018-03-30

Abstract: OBJECTIVE: The present study was designed to investigate the possible mechanisms of proanthocyanidin-mediated inhibition in lipopolysaccharide (LPS)-induced activation of microglial BV2 cells. METHODS: An inflammation cell model was produced in BV2 cells which were treated with LPS (1.0 μg/mL). In addition,cells were treated with proanthocyanidins (0.1,0.5,2.5,10.0 μg/mL) prior to LPS exposure and MTT assay was used to detect the viability of BV2 cells. The level of inflammatory cytokines TNF-α,IL-1β and IL-6 were examined by ELISA method. TLR4 and p38,p-p38 MAPK protein expressions were examined by the Western blot analysis. RESULTS: Compared with the control group,LPS (1.0 μg/mL) significantly increased the expression of TLR4 and p-p38 protein as well as the release of inflammatory mediator TNF-α,IL-1β and IL-6 (P < 0.05). Proanthocyanidin significantly inhibited LPS-induced production of inflammatory mediators in a dose-dependent manner (P < 0.05). Moreover,PC significantly inhibited the phosphorylation of p38 and TLR4 expression (P < 0.05). CONCLUSION: Proanthocyanidin inhibited inflammatory mediator expression by suppressing TLR4 mediated p38 MAPK signaling pathways in LPS-stimulated BV2 cells.

Key words: proanthocyanidin, lipopolysaccharide, microglia, TLR4, p38 MAPK

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