Jaceosidin Protects L929 Fibroblast Cells by Down-Regulation of Proinflammatory Cytokines and Attenuation of Oxidative Stress-Induced Impairment of Cell Proliferation and Migration

Abstract

Aim: Oxidative stress has been a significant factor in wound-healing pathophysiology for a long time. Antioxidants, especially natural compounds, have recently been emphasized in instructions for wound healing treatments. Jaceosidin (JACE), a flavone derived from Artemisia princeps, is a potent antioxidant. This study aims to investigate JACE’s anti-inflammatory and antioxidant properties and its capacity to improve the effects of in vitro wound healing. Methods: Wound healing activities have been tested using cell proliferation and migration in vitro assays in the mouse fibroblast cell line L929. The concentration of hydrogen peroxide (H2O2-0.5 mM) has been used to induce the oxidative stress model. Tumor necrosis factor-alpha (TNF-α) and nuclear factor (NF-) have been investigated as inflammatory indicators. Antioxidant activity has been checked using total antioxidant status (TAS) and total oxidant status (TOS) tests. Results: JACE has significantly increased the proliferation of fibroblasts dose-dependent manner. It has enhanced the cell migration rate of fibroblasts compared with the H2O2 group. JACE at a concentration of 50 and 100 μM has significantly decreased TOS and oxidative stress index (OSI) levels and increased TAS levels. The anti-inflammatory mechanism of JACE has involved down-regulation of the mRNA expressions of the NF- and TNF-α in a dose-dependent manner. Conclusions: JACE has beneficial impacts on fibroblast viability and migration qualities through antioxidative actions and down-regulating proinflammatory cytokines through anti-inflammatory effects to promote wound healing. The present study shows that JACE may help to increase the range of available treatments for woundhealing by reducing inflammation and oxidative stress.