期刊
JOURNAL OF MOLECULAR NEUROSCIENCE
卷 56, 期 4, 页码 858-867出版社
HUMANA PRESS INC
DOI: 10.1007/s12031-015-0526-5
关键词
SIRT1; Resveratrol; MicroRNA; Microglia; Lipopolysaccharide (LPS); Sepsis; Septic encephalopathy (SE)
资金
- Shaanxi Province Science and Technology Research and Development Program [2013 K12-01-07]
- National Natural Science Foundation of China [30600524, 81071990, 81201758]
- Science and Technology Planning Project of Guangdong Province [2012A030400055, 2010B080701088, 2011B080701096, 2011B031800184]
- Science and Technology Application infrastructure projects of Guangzhou [2011 J410010, 2011 J4300066]
Microglia activation plays an important role in neuroinflammation. Sirtuin1 (SIRT1) has been shown to play a role in regulation of inflammation. Resveratrol, a potent SIRT1 activator, has anti-inflammation property. MicroRNA (miRNA or miR) related to inflammation pathways has been shown to be a promising therapeutic approach for septic encephalopathy (SE). The miR mediated mechanism of regulation of SIRT1 expression in encephalitis. However, the mechanism of was unknown. To address this question, we investigated whether miRNAs and resveratrol regulate the SIRT1 and the functional changes of mice microglia cell lines pre-treated with or without lipopolysaccharide (LPS). The research about direct role of miR-204 and resveratrol on expression of SIRT1 in mice microglia cell lines (N9 and BV2) pre-treated with or without LPS had been performed. Mice microglia cell lines were transfected with miR-204 mimics and inhibitors or treated with resveratrol, and the effects on cell growth, proliferation, and apoptosis of cells were assessed. LPS induced inflammation and activation of mice microglia. Through overexpression of SIRT1, resveratrol, and inhibitor of miR-204 inhibited inflammation process, proliferation of mice microglia cells and promoted its apoptosis. We identified if resveratrol and miR-204 could repress inflammation process and proliferation of mice microglia cell through promoting the expression of SIRT1.
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