Abstract
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 Arctium lappa, 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. Taken together, we demonstrated that arctigenin may act as a suitable adjunct therapy for OSF.
Highlights
Oral submucous fibrosis (OSF) is a premalignant disorder [1] characterized by chronic inflammation and progressive accumulation of collagen in the oral cavity
In order to test whether arctigenin was able to impede the effect of arecoline on buccal mucosal fibroblasts (BMFs), we examined a variety of phenotypic analyses of myofibroblast activities
The arecoline-induced enhancement of cell motility was avoided in the presence of arctigenin as assessed by invasion (Figure 3A) and wound healing (Figure 3B) assays. These findings indicate that arctigenin may possess the potential to obviate the excessive activation of myofibroblasts caused by areca nut
Summary
Oral submucous fibrosis (OSF) is a premalignant disorder [1] characterized by chronic inflammation and progressive accumulation of collagen in the oral cavity. The common clinical symptoms include blanched mucosa and stiffness of the mouth, leading to limited food consumption, impaired speaking ability, and difficulty of maintaining oral hygiene. These symptoms cause significant social, economic, and quality-of-life burdens to patients. It is known that TGF-β drives fibroblast–myofibroblast transdifferentiation via the induction of a contractile phenotype and up-regulation of α-SMA. Those alterations are related to the increase in collagen gene expression and are regulated by Smad proteins [9]. A therapeutic strategy that targets the TGF-β pathway in myofibroblast transdifferentiation may serve as a promising approach
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