Effect of Chinese Herbal Compound Naofucong (脑复聪) on theInflammatory Process Induced by High Glucose in BV-2 Cells  

作　　者：景光婵 张孟仁 纪超 左萍萍 刘玉琴 顾蓓 

机构地区：[1]Department of Traditional Chinese Medicine, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100730, China [2]Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences and School of Basic Medicine, Peking Union Medical College, Beijing 100005, China

出　　处：《Chinese Journal of Integrative Medicine》2016年第11期832-839,共8页中国结合医学杂志（英文版）

基　　金：Supported by Beijing Natural Science Foundation(No.7142129);Beijing Science and Technology Project of Traditional Chinese Medicine(No.JJ2014-50),China

摘　　要：Objective: To determine the effect of medicated serum of Chinese herbal compound Naofucong(脑复聪, NFC) on the microglia BV-2 cells viability and the transcription and expression of interleukin-6(IL-6) and tumor necrosis factor α(TNF-α) in microglia BV-2 cells to further explore the mechanisms underlying the protective effect of NFC on inflammatory process induced by high glucose. Methods: The microglia BV-2 cells incubated in vitrowere divided into different groups: the control group(25 mmol/L glucose), the model group(75 mmol/L glucose), high glucose media containing different dose medicated serum of NFC. After being cultured for 24 h, changes in IL-6 and TNF-α were measured by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay. The expression of surface marker CD11 b of activated microglia was measured by confocal laser scanning microscope and Western blot. Nuclear factor-κB(NF-κB) p-p65 expression was analyzed by Western blot. Results: The model group obviously increased the expression of microglial surface marker CD11 b and NF-κB p-p65(all P<0.01), induced a significant up-regulation of release and the m RNA expression of IL-6 and TNF-α(P<0.01 or P<0.05). The medicated serum of NFC could obviously down-regulate the transcription and expression of surface marker CD11 b and NF-κB p-p65(all P<0.01), and inhibit the m RNA and protein expression(P<0.01 or P<0.05) of inflammatory cytokines, such as IL-6 and TNF-α, in microglia BV-2 cells cultured with high glucose for 24 h. Conclusions: The inhibition of microglial activation and IL-6 and TNF-α expression induced by high glucose may at least partly explain NFC therapeutic effects on diabetes-associated cognitive decline diseases. Its underlying mechanism could probably be related to the inhibition of NFC on NF-κB phosphorylation.Objective: To determine the effect of medicated serum of Chinese herbal compound Naofucong(脑复聪, NFC) on the microglia BV-2 cells viability and the transcription and expression of interleukin-6(IL-6) and tumor necrosis factor α(TNF-α) in microglia BV-2 cells to further explore the mechanisms underlying the protective effect of NFC on inflammatory process induced by high glucose. Methods: The microglia BV-2 cells incubated in vitrowere divided into different groups: the control group(25 mmol/L glucose), the model group(75 mmol/L glucose), high glucose media containing different dose medicated serum of NFC. After being cultured for 24 h, changes in IL-6 and TNF-α were measured by quantitative real-time polymerase chain reaction and enzyme-linked immunosorbent assay. The expression of surface marker CD11 b of activated microglia was measured by confocal laser scanning microscope and Western blot. Nuclear factor-κB(NF-κB) p-p65 expression was analyzed by Western blot. Results: The model group obviously increased the expression of microglial surface marker CD11 b and NF-κB p-p65(all P<0.01), induced a significant up-regulation of release and the m RNA expression of IL-6 and TNF-α(P<0.01 or P<0.05). The medicated serum of NFC could obviously down-regulate the transcription and expression of surface marker CD11 b and NF-κB p-p65(all P<0.01), and inhibit the m RNA and protein expression(P<0.01 or P<0.05) of inflammatory cytokines, such as IL-6 and TNF-α, in microglia BV-2 cells cultured with high glucose for 24 h. Conclusions: The inhibition of microglial activation and IL-6 and TNF-α expression induced by high glucose may at least partly explain NFC therapeutic effects on diabetes-associated cognitive decline diseases. Its underlying mechanism could probably be related to the inhibition of NFC on NF-κB phosphorylation.

关 键 词：high glucose MICROGLIA inflammatory cytokine Chinese herbal compound Naofucong 

分 类 号：R285[医药卫生—中药学]