荜澄茄素通过抑制转化生长因子-β/Smad2/3 信号通路抑制槟榔碱诱导的口腔纤维组织生成。
Honokiol inhibits arecoline-induced oral fibrogenesis through transforming growth factor-β/Smad2/3 signaling inhibition.
机构信息
School of Dentistry, Chung Shan Medical University, Taichung, Taiwan; Department of Dentistry, Chung Shan Medical University Hospital, Taichung, Taiwan.
Division of Oral and Maxillofacial Surgery, Department of Dentistry, Wan Fang Hospital, Taipei, Taiwan; School of Dentistry, College of Oral Medicine, Taipei Medical University, Taipei, Taiwan.
出版信息
J Formos Med Assoc. 2021 Nov;120(11):1988-1993. doi: 10.1016/j.jfma.2021.04.012. Epub 2021 May 9.
BACKGROUND/PURPOSE: The habit of areca nut chewing has been regarded as an etiological factor of precancerous oral submucous fibrosis (OSF). In the present study, we aimed to evaluate the anti-fibrosis effect of honokiol, a polyphenolic component derived from Magnolia officinalis.
METHODS
The cytotoxicity of honokiol was tested using normal and fibrotic buccal mucosal fibroblasts (fBMFs) derived from OSF tissues. Collagen gel contraction, Transwell migration, invasion, and wound healing capacities were examined. Besides, the expression of TGF-β/Smad2 signaling as well as α-SMA and type I collagen were measured as well.
RESULTS
Honokiol exerted higher cytotoxicity of fBMFs compared to normal cells. The arecoline-induced myofibroblast activities, including collagen gel contractility, cell motility and wound healing capacities were all suppressed by honokiol treatment. In addition, the expression of the TGF-β/Smad2 pathway was downregulated along with a lower expression of α-SMA and type I collagen in honokiol-receiving cells.
CONCLUSION
Our data suggest that honokiol may be a promising compound to alleviate the progression of oral fibrogenesis and prevent the transformation of OSF oral epithelium into cancer.
背景/目的：槟榔咀嚼习惯被认为是癌前口腔黏膜下纤维性变（OSF）的病因之一。本研究旨在评估厚朴酚（一种源自Magnolia officinalis 的多酚成分）的抗纤维化作用。
方法
使用源自 OSF 组织的正常和纤维化颊黏膜成纤维细胞（fBMFs）测试厚朴酚的细胞毒性。检测胶原凝胶收缩、Transwell 迁移、侵袭和伤口愈合能力。此外，还测量了 TGF-β/Smad2 信号通路以及α-SMA 和 I 型胶原的表达。
结果
与正常细胞相比，厚朴酚对 fBMFs 的细胞毒性更高。厚朴酚处理可抑制槟榔碱诱导的成肌纤维细胞活性，包括胶原凝胶收缩性、细胞迁移和伤口愈合能力。此外，厚朴酚处理的细胞中 TGF-β/Smad2 通路的表达下调，α-SMA 和 I 型胶原的表达降低。
结论
我们的数据表明，厚朴酚可能是一种有前途的化合物，可以缓解口腔纤维化的进展，并防止 OSF 口腔上皮向癌症转化。
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