IR@PKUHSC  > 北京大学第三临床医学院
学科主题临床医学
Tetrandrine Suppresses Lipopolysaccharide-Induced Microglial Activation by Inhibiting NF-kappa B and ERK Signaling Pathways in BV2 Cells
Dang, Yalong1,2,3; Xu, Yongsheng2,3; Wu, Wentao2; Li, Weiyi2,3; Sun, Yanran3; Yang, Jing1; Zhu, Yu1; Zhang, Chun2,3
刊名PLOS ONE
2014-08-12
DOI10.1371/journal.pone.0102522
9期:8
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]RETINAL GANGLION-CELLS ; TUMOR-NECROSIS-FACTOR ; OPTIC-NERVE HEAD ; OPEN-ANGLE GLAUCOMA ; FOCAL CEREBRAL-ISCHEMIA ; FACTOR-ALPHA ; MOUSE MODEL ; GENE-EXPRESSION ; NEUROPROTECTION ; INFLAMMATION
英文摘要

Background and Objective: Tetrandrine (TET) is a bisbenzylisoquinoline alkaloid extracted from Stephania tetrandra Moore. Recent studies have suggested that TET can reduce the inflammatory response in microglia, but the mechanisms remain unclear. The aim of this study is to investigate whether TET can inhibit lipopolysaccharide (LPS)-induced microglial activation and clarify its possible mechanisms.

Study Design/Materials and Methods: Cell viability assays and cell apoptosis assays were used to determine the working concentrations of TET. Then, BV2 cells were seeded and pretreated with TET for 2 h. LPS was then added and incubated for an additional 24 hours. qRT-PCR and ELISA were used to measure the mRNA or protein levels of IL1 beta and TNF alpha. Western blotting was utilized to quantify the expression of CD11b and cell signaling proteins.

Results: TET at optimal concentrations (0.1 mu M, 0.5 mu M or 1 mu M) did not affect the cell viability. After TET pretreatment, the levels of IL1 beta and TNF alpha (both in transcription and translation) were significantly inhibited in a dose-dependent manner. Further studies indicated that phospho-p65, phospho-IKK, and phospho-ERK 1/2 expression were also suppressed by TET.

Conclusions: Our results indicate that TET can effectively suppress microglial activation and inhibit the production of IL1 beta and TNF alpha by regulating the NF-kappa B and ERK signaling pathways. Together with our previous studies, we suggest that TET would be a promising candidate to effectively suppress overactivated microglia and alleviate neurodegeneration in glaucoma.

语种英语
WOS记录号WOS:000341230400005
引用统计
被引频次:16[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/53482
专题北京大学第三临床医学院
北京大学第三临床医学院_临床干细胞研究中心
作者单位1.Zhengzhou Univ, Affiliated Hosp 1, Dept Ophthalmol, Zhengzhou 450052, Henan Province, Peoples R China
2.Peking Univ, Hosp 3, Clin Stem Cell Res Ctr, Beijing 100871, Peoples R China
3.Peking Univ, Hosp 3, Dept Ophthalmol, Beijing 100871, Peoples R China
推荐引用方式
GB/T 7714
Dang, Yalong,Xu, Yongsheng,Wu, Wentao,et al. Tetrandrine Suppresses Lipopolysaccharide-Induced Microglial Activation by Inhibiting NF-kappa B and ERK Signaling Pathways in BV2 Cells[J]. PLOS ONE,2014,9(8).
APA Dang, Yalong.,Xu, Yongsheng.,Wu, Wentao.,Li, Weiyi.,Sun, Yanran.,...&Zhang, Chun.(2014).Tetrandrine Suppresses Lipopolysaccharide-Induced Microglial Activation by Inhibiting NF-kappa B and ERK Signaling Pathways in BV2 Cells.PLOS ONE,9(8).
MLA Dang, Yalong,et al."Tetrandrine Suppresses Lipopolysaccharide-Induced Microglial Activation by Inhibiting NF-kappa B and ERK Signaling Pathways in BV2 Cells".PLOS ONE 9.8(2014).
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