Coniferaldehyde inhibits LPS-induced apoptosis through the PKC α/β II/Nrf-2/HO-1 dependent pathway in RAW264.7 macrophage cells

被引：22
|
作者：
Kim, Ki Mo [1 ]
Heo, Deok Rim [1 ]
Kim, Young-A. [1 ]
Lee, Jun [1 ]
Kim, No Soo [1 ]
Bang, Ok-Sun [1 ]
机构：
[1] Korea Inst Oriental Med, KM Convergence Res Div, 1672 Yuseong Daero, Daejeon 305811, South Korea
来源：
ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY | 2016年 / 48卷
关键词：
Coniferaldehyde; PKC alpha/beta II; Nrf-2; HO-1; Apoptosis; Macrophages; HEME OXYGENASE-1 EXPRESSION; NITRIC-OXIDE SYNTHASE; ACID PHENETHYL ESTER; FACTOR-KAPPA-B; OXIDATIVE STRESS; SIGNALING PATHWAY; GENE-EXPRESSION; NO PRODUCTION; HEPG2; CELLS; LIPOPOLYSACCHARIDE;
D O I：
10.1016/j.etap.2016.10.016
中图分类号：
X [环境科学、安全科学];
学科分类号：
08 ; 0830 ;
摘要：
Coniferaldehyde (CA) exerts anti-inflammatory properties by inducing heme oxygenase-1 (HO-1). To define the regulation mechanism by which CA induces a cytoprotective function and HO-1 expression, the up-stream regulations involved in the activation of nuclear transcription factor-erythroid 2-related factor (Nrf)-2/HO-1 pathway were investigated. CA dramatically increased the Nrf-2 nuclear translocation and HO-1 expression. Lipopolysaccharide (LPS)-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase (COX)-2, and cell death were down-regulated by CA, which were reversed by inhibition of HO-1 activity. Furthermore, CA specifically enhanced the phosphorylation of protein kinase C (PKC) alpha/beta II. Selective inhibition of PKC alpha/beta II using Go6976 or siRNA abolished the CA-induced Nrf-2/HO-1 signaling, and consequently suppressed the cytoprotective activity of CA on the LPS-induced cell death. Together, our results elucidate the regulatory mechanism of PKC alpha/beta II as the upstream molecule of Nrf-2 required for HO-1 expression during CA-induced anti-inflammatory cytoprotective function in LPS stimulated macrophages. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码：85 / 93
页数：9
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