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Ramulus Cinnamomi extract attenuates neuroinflammatory responses via downregulating TLR4/MyD88 signaling pathway in BV2 cells 被引量:5

Ramulus Cinnamomi extract attenuates neuroinflammatory responses via downregulating TLR4/My D88 signaling pathway in BV2 cells
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摘要 Ramulus Cinnamomi(RC), a traditional Chinese herb, has been used to attenuate inflammatory responses. The purpose of this study was to investigate the effect of RC extract on lipopolysaccharide(LPS)-induced neuroinflammation in BV2 microglial cells and the underlying mechanisms involved. BV2 cells were incubated with normal medium(control group), LPS, LPS plus 30 μg/m L RC extract, or LPS plus 100 μg/m L RC extract. The BV2 cell morphology was observed under an optical microscope and cell viability was detected by MTT assay. Nitric oxide level in BV2 cells was detected using Griess regents, and the levels of interleukin-6, interleukin-1β, and tumor necrosis factor α in BV2 cells were determined by ELISA. The expression levels of cyclooxygenase-2, Toll-like receptor 4 and myeloid differentiation factor 88 proteins were detected by western blot assay. Compared with the LPS group, both 30 and 100 μg/mL RC extract had no significant effect on the viability of BV2 cells. The levels of nitric oxide, interleukin-6, interleukin-1β and tumor necrosis factor α in BV2 cells were all significantly increased after LPS induction, and the levels were significantly reversed after treatment with 30 and 100 μg/mL RC extract. Furthermore, RC extract significantly inhibited the protein expression levels of cyclooxygenase-2, Toll-like receptor 4 and myeloid differentiation factor 88 in LPS-induced BV2 cells. Our findings suggest that RC extract alleviates neuroinflammation by downregulating the TLR4/My D88 signaling pathway. Ramulus Cinnamomi (RC), a traditional Chinese herb, has been used to attenuate inflammatory responses. The purpose of this study was to investigate the effect of RC extract on lipopolysaccharide (LPS)-induced neuroinflammation in BV2 microglial cells and the underlying mechanisms involved. BV2 cells were incubated with normal medium (control group), LPS, LPS plus 30 pg/mL RC extract, or LPS plus 100 pg/mL RC extract. The BV2 cell morphology was observed under an optical microscope and cell viability was detected by MTT assay. Nitric oxide level in BV2 cells was detected using Griess regents, and the levels of interleukin-6, interleukin-1 β, and tumor necrosis factor u in BV2 cells were determined by ELISA. The expression levels of cyclooxygenase-2, Toll-like receptor 4 and myeloid differentiation factor 88 proteins were detected by western blot assay. Compared with the LPS group, both 30 and 100 μg/mL RC extract had no significant effect on the viability of BV2 cells. The levels of nitric oxide, interleukin-6, interleukin-1β and tumor necrosis factor ct in BV2 cells were all significantly increased after LPS induction, and the levels were significantly reversed after treatment with 30 and 100 μg/mL RC extract. Furthermore, RC extract significantly inhibited the protein expression levels of cyclooxygenase-2, Toll-like receptor 4 and myeloid differentiation factor 88 in LPS-induced BV2 cells. Our findings suggest that RC extract alleviates neuroinflammation by downregulating the TLR4/MyD88 signaling pathway.
出处 《Neural Regeneration Research》 SCIE CAS CSCD 2017年第11期1860-1864,共5页 中国神经再生研究(英文版)
基金 supported by a grant from the National Natural Science Foundation of China,No.81473383 a grant from the Medical and Health Innovation Project of Chinese Academy of Medical Sciences,No.2016-I2M-3-007 a grant from Key Project of New-Drugs Creation of Science and Technology of China,No.2012ZX09103101-078 and 2017ZX09101003-003-019
关键词 nerve regeneration Ramulus Cinnamomi BV2 cells LIPOPOLYSACCHARIDE NEUROINFLAMMATION pro-inflammatory factors TLR4/My D88 signaling pathway nitric oxide INTERLEUKIN-6 INTERLEUKIN-1Β tumor necrosis factor α neuronal regeneration nerve regeneration Ramulus Cinnamomi BV2 cells lipopolysaccharide neuroinflammation pro-inflammatory factors TLR4/ MyD88 signaling pathway nitric oxide interleukin-6 interleukin-1β tumor necrosis factor a neuronal regeneration
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