The role of wogonin in controlling SOCS3 expression in neuronal cells

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WEB OF SCIENCE

2
Citations

SCOPUS

2

초록

The mechanism underlying the wogonin-mediated increase in the expression of suppressor of cytokine signaling 3 (SOCS3) is unclear. Promoter deletion assay results revealed that wogonin-induced SOCS3 expression is dependent on the AP-1 consensus sequences and two STAT responsive elements (TTACAAGAA and TTCCAGGAA) in the 5'-flanking region of the SOCS3 gene in SH-SY5Y cells. Wogonin-induced SOCS3 expression was blocked by inhibitors of PI3K, Akt, Raf, p38, JNK, MEK, and STAT3, respectively. However, JAK2 inhibitors did not inhibit wogonin-induced SOCS3 expression. These results indicate that SOCS3-inducing effect of wogonin is caused by the activation of PI3K-mediated MAPK signaling pathways (Akt, ERK1/2, p38, and JNK), and the subsequent activation of AP-1 consensus sequences and STAT responsive elements in SH-SY5Y cells. (C) 2014 Elsevier Inc. All rights reserved.

키워드

Wogonin; SOCS3; Neuroinflammation; PI3K; AP1; STAT3; CYTOKINE SIGNALING 3; CEREBRAL-ARTERY OCCLUSION; KAPPA-B; INFLAMMATORY ARTHRITIS; ENDOTHELIAL-CELLS; SUPPRESSOR; INHIBITION; APOPTOSIS; MACROPHAGES; TRANSDUCER
제목
The role of wogonin in controlling SOCS3 expression in neuronal cells
저자
Nam, Kung-Woo; Chae, Sungwook; Song, Ho-Yeon; Mar, Woongchon; Han, Man-Deuk
DOI
10.1016/j.bbrc.2014.07.018
발행일
2014-08-08
유형
Article
저널명
Biochemical and Biophysical Research Communications
권
450
호
4
페이지
1518 ~ 1524