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厚朴酚通过阻断大鼠主动脉平滑肌细胞中ERK信号通路的NF-κB激活来抑制TNF-α诱导的迁移和基质金属蛋白酶表达。

Honokiol suppresses TNF-α-induced migration and matrix metalloproteinase expression by blocking NF-κB activation via the ERK signaling pathway in rat aortic smooth muscle cells.

作者信息

Zhu Xiaoying, Wang Zhansheng, Hu Cuizhu, Li Zhao, Hu Jian

机构信息

Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, People's Republic of China; Department of Cardiology, The General Hospital of Benxi Iron and Steel Co. Ltd., The Fifth Affiliated Hospital of China Medical University, Benxi, Liaoning 117000, People's Republic of China.

Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang, Liaoning 110001, People's Republic of China.

出版信息

Acta Histochem. 2014 May;116(4):588-95. doi: 10.1016/j.acthis.2013.11.005. Epub 2013 Dec 20.

Abstract

Honokiol, a small-molecule polyphenol derived and isolated from the Chinese medicinal herb Magnolia officinalis, has been shown to possess a wide range of pharmacological activities. In the present study, we aimed to investigate the effects of honokiol on tumor necrosis factor-α (TNF-α)-induced migration in rat aortic smooth muscle cells (RASMCs). We found that honokiol inhibited TNF-α-induced RASMC proliferation and migration in a dose-dependent manner. At the molecular level, pretreatment with honokiol blocked TNF-α-induced protein expression of matrix metalloproteinase (MMP)-2 and MMP-9, nuclear factor (NF)-κB activation, and extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation. Moreover, NF-κB inhibitor (BAY 11-7028) and ERK inhibitor (U0126) also mimicked the inhibitory effects of honokiol in TNF-α-treated RASMCs. In conclusion, these results indicate that honokiol suppresses TNF-α-induced migration and MMP expression by blocking NF-κB activation via the ERK signaling pathway in RASMCs. Our findings support honokiol as a promising novel agent for the prevention and treatment of atherosclerosis.

摘要

厚朴酚是一种从中药材厚朴中提取和分离出的小分子多酚,已被证明具有广泛的药理活性。在本研究中,我们旨在研究厚朴酚对肿瘤坏死因子-α(TNF-α)诱导的大鼠主动脉平滑肌细胞(RASMCs)迁移的影响。我们发现厚朴酚以剂量依赖性方式抑制TNF-α诱导的RASMCs增殖和迁移。在分子水平上,用厚朴酚预处理可阻断TNF-α诱导的基质金属蛋白酶(MMP)-2和MMP-9的蛋白表达、核因子(NF)-κB激活以及细胞外信号调节激酶1/2(ERK1/2)磷酸化。此外,NF-κB抑制剂(BAY 11-7028)和ERK抑制剂(U0126)也模拟了厚朴酚对TNF-α处理的RASMCs的抑制作用。总之,这些结果表明厚朴酚通过在RASMCs中经由ERK信号通路阻断NF-κB激活来抑制TNF-α诱导的迁移和MMP表达。我们的研究结果支持厚朴酚作为一种有前景的新型药物用于动脉粥样硬化的预防和治疗。

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