Protective effect of wogonin on proinflammatory cytokine generation via Jak1/3-STAT1/3 pathway in lipopolysaccharide stimulated BV2 microglial cells. (October 2015)

• Record Type: Journal Article
• Authors: Yeh, Chung-Hsin; Shih, Hung-Che; Hong, Hui-Mei; Lee, Shiuan-Shinn; Yang, Ming-Ling; Chen, Chun-Jung; Kuan, Yu-Hsiang
• Is Part Of: Toxicology and industrial health. Volume 31:Number 10(2015)
• Page Start: 960
• Page End: 966
• Publication Date: 2015-10
• Subjects: Wogonin -- BV2 microglial cells -- STAT -- Jak -- antiinflammation; Toxicology, Experimental -- Periodicals; Industrial toxicology -- Periodicals; 615.9
• DOI: 10.1177/0748233713485886
• Languages: English
• ISSNs: 0748-2337

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.