Protective effect of wogonin on proinflammatory cytokine generation via Jak1/3-STAT1/3 pathway in lipopolysaccharide stimulated BV2 microglial cells

doi:10.1177/0748233713485886

中山醫學大學機構典藏 CSMUIR > 健康管理學院 > 公共衛生學系暨碩士班 > 期刊論文 > Item 310902500/17843

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题名:	Protective effect of wogonin on proinflammatory cytokine generation via Jak1/3-STAT1/3 pathway in lipopolysaccharide stimulated BV2 microglial cells
作者:	Yeh, Chung-Hsin Shih, Hung-Che Hong, Hui-Mei Lee, Shiuan-Shinn Yang, Ming-Ling Chen, Chun-Jung Kuan, Yu-Hsiang
贡献者:	中山醫大
日期:	2013-04
上传时间:	2017-06-28T08:18:04Z (UTC)
出版者:	Toxicol Ind Health
ISSN:	0748-2337
摘要:	Abstract Wogonin is a flavonoid compound which exhibits antioxidation, anti-inflammation, neuroprotection, and antitumorgenesis functions. However, the mechanism of how wogonin reduces proinflammatory cytokine generation in activated microglia is unclear. At present, we found wogonin inhibited lipopolysaccharide (LPS)-/interferon-γ (INF-γ)-induced generation of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α). Wogonin exhibited parallel inhibition on LPS-/INF-γ-induced expression of IL-6 and TNF-α messenger RNA at the same concentration range. LPS-/INF-γ-induced phosphorylation of signal transduction and transcription 1 and 3 (STAT1/3) were also inhibited by wogonin. Although wogonin expressed only weak inhibitory effect on LPS-/INF-γ-induced phosphorylation of Janus kinase-2 (Jak-2) and tyrosine kinase (Tyk)-2, it significantly attenuated the phosphorylation of Jak-1 and Jak-3. These results indicated that the blockade of IL-6 and TNF-α production by wogonin in LPS-/INF-γ-stimulated BV2 microglial cells was attributed mainly to the interference in Jak-1/-3-STAT1/3 signaling pathway.
URI:	http://dx.doi.org/10.1177/0748233713485886 https://ir.csmu.edu.tw:8080/ir/handle/310902500/17843
關聯:	Toxicol Ind Health. 2015 Oct;31(10):960-6.
显示于类别:	[公共衛生學系暨碩士班] 期刊論文

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