Anti-fibrotic activity of licorice extract in comparison with colchicine on areca nut-induced fibroblasts

Abstract

Objective: Oral submucous fibrosis (OSMF) is a debilitating chronic disease of the oral cavity with a high potential for malignant transformation. The main etiological agent attributed to the development of OSMF is the use of smokeless tobacco products like areca nut. There is no known cure for the disease. Current modalities of treatment do not provide a complete cure and often prove invasive for the patient. Herbal preparations using natural compounds and medicinal plant extracts have long since been used in India, as an acceptable, noninvasive and cost-effective method in the treatment of various diseases. Hence, the present study aims to assess the anti-fibrotic effect of licorice in comparison with colchicine on areca nut-induced fibroblasts. Materials and Methods: Extracts of areca nut, licorice and colchicine were prepared in accordance with established protocols. Human fibroblast cell lines were procured from ATCC®(PSC-201-018). Fibroblast cultures were established, and upon reaching confluence the cells were subjected to the 25 μg/ml areca nut extract for 24 h to induce fibrosis, with CCl4 used as control fibrosing agent. The areca nut and CCl4 induced cells were then subjected to varying concentration of the test antifibrotic agent, licorice extract for the periods of 24 and 48 h, with colchicine used as positive control. Total collagen quantification was done using spectrophotometry. Results: Collagen accumulation decreased with increase in the concentration of licorice extract with maximum reduction seen at 200 μg/ml. Kruskal–Wallis test was done to analyze the difference in collagen accumulation. Analysis revealed that the P < 0.05 for both periods in both the areca and CCl4 induced cell lines following the addition of licorice extract. The data were found to be statistically significant. Conclusion: The current study proves the antifibrotic efficacy of licorice in areca nut induced cell lines and hence, this agent can be used for the therapeutic management of OSMF.

A Chinese classical prescription Maimendong decoction in treatment of pulmonary fibrosis: an overview

“…Research has shown that glycyrrhiza and some of its extracts possess anti-PF effects ( Ghorashi et al, 2016 ). One of its saponin components, glycyrrhizic acid, has been found to inhibit the increase of TGF-β1, IL-17, and p-Smad2 expression in mice with PF, thus exerting anti-fibrotic effects by suppressing the expression of transforming growth factor and inflammatory factors ( Li et al, 2018 ; James et al, 2022 ). Another compound, licochalcone A, a phenolic chalcone derived from glycyrrhiza significantly inhibits TGF-β-induced transformation of fibroblast MRC-5 cells and reduces the expression of α-α-SMA and fibronectin (FN) in lung tissue.…”

The Power of Licorice (Radix glycyrrhizae) to Improve Oral Health: A Comprehensive Review of Its Pharmacological Properties and Clinical Implications

“…Licorice was suggested as a treatment for OSF because it demonstrated antifibrotic effectiveness in human fibroblast cell lines [72].…”

Possibilities of Plant Preparations Use for Collagen Structure and Metabolism Disturbances Correction: Modern State of Problem

“…Persimmon leaf (Diospyros kaki folium) extracts also demonstrate such ability with simultaneous activation of elastase [26]. Areca nut extracts cause disruption of the equilibrium between matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMP) [27].…”

“…Alkaloids from areca nut are the most important biologically for collagen metabolism regulation whilst tannin may have a synergistic role. These chemicals appear to interfere with the molecular processes of deposition and/or degradation of extracellular matrix molecules such as collagen [27,68].…”

“…In vitro studies on human fibroblasts with chemically purified arecoline established its ability to increase collagen formation that is also demonstrable histologically in human fibrosis tissues. Increased collagen synthesis could be a result of not only expression of collagen genes, but also of disruption of the equilibrium between matrix metalloproteinases and their tissue inhibitors [27].…”