Article Publish Status: FREE
Abstract Title:

Arctigenin Reduces Myofibroblast Activities in Oral Submucous Fibrosis by LINC00974 Inhibition.

Abstract Source:

Int J Mol Sci. 2019 Mar 16 ;20(6). Epub 2019 Mar 16. PMID: 30884781

Abstract Author(s):

Ching-Yeh Lin, Pei-Ling Hsieh, Yi-Wen Liao, Chih-Yu Peng, Cheng-Chia Yu, Ming-Yi Lu

Article Affiliation:

Ching-Yeh Lin


Oral submucous fibrosis (OSF) is an oral precancerous condition associated with the habit of areca nut chewing and the TGF-β pathway. Currently, there is no curative treatment to completely heal OSF, and it is imperative to alleviate patients' symptoms and prevent it from undergoing malignant transformation. Arctigenin, a lignan extracted from, has been reported to have a variety of pharmacological activities, including anti-fibrosis. In the present study, we examined the effect of arctigenin on the cell proliferation of buccal mucosal fibroblasts (BMFs) and fibrotic BMFs (fBMFs), followed by assessment of myofibroblast activities. We found that arctigenin was able to abolish the arecoline-induced collagen gel contractility, migration, invasion, and wound healing capacities of BMFs and downregulate the myofibroblast characteristics of fBMFs in a dose-dependent manner. Most importantly, the production of TGF-β in fBMFs was reduced after exposure to arctigenin, along with the suppression of p-Smad2, α-smooth muscle actin, and type I collagen A1. In addition, arctigenin was shown to diminish the expression of LINC00974, which has been proven to activate TGF-β/Smad signaling for oral fibrogenesis. Takentogether, we demonstrated that arctigenin may act as a suitable adjunct therapy for OSF.

Study Type : In Vitro Study
Additional Links
Pharmacological Actions : Anti-Fibrotic : CK(924) : AC(463)

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