Jaceosidin protects L929 fibroblast cells by down-regulation of proinflammatory cytokines and attenuation of oxidative stress-induced impairment of cell proliferation and migration

Busra Dincer; Azat Cekdar Gundogmus; Irfan Cinar

doi:10.30714/j-ebr.2023.188

Busra Dincer Department of Pharmacology, Ondokuz Mayıs University, Faculty of Pharmacy, Samsun, Türkiye http://orcid.org/0000-0002-3365-7741
Azat Cekdar Gundogmus Department of Pharmacology, Erzincan Binali Yıldırım University, Faculty of Pharmacy, Erzincan, Türkiye http://orcid.org/0009-0007-6681-2414
Irfan Cinar Department of Pharmacology, Kastamonu University, Faculty of Medicine, Kastamonu, Türkiye http://orcid.org/0000-0002-9826-2556

DOI: https://doi.org/10.30714/j-ebr.2023.188

Keywords: Wound-healing, jaceosidin, antioxidant, fibroblast L929 cells, oxidative stress, hydrogen peroxide

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-kb) 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-kb 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 wound-healing by reducing inflammation and oxidative stress.