Madecassic acid protects human periodontal ligament fibroblasts against hydrogen peroxide-induced cell damage by maintaining mitochondrial membrane potential

• Published in: Molecular & cellular toxicology 2022, 18(1), , pp.81-90
• Main Authors: Jin, Yuqin, Li, Jialing, Ding, Liang, Zhao, Qing, Song, Yuxian, Li, Guifeng, Ji, Jun, Ni, Yanhong, Hu, Qingang
• Format: Article
• Language: English
• Subjects: Biomedical and Life Sciences; Cell Biology; Life Sciences; Original Article; Pharmacology/Toxicology; 생물학
• ISSN: 1738-642X; 2092-8467
• DOI: 10.1007/s13273-021-00174-1

Background Oxidative stress is involved in the pathogenesis of various inflammatory diseases, such as periodontitis. When periodontitis occurs, reactive oxygen species (ROS) are overproduced and cannot be balanced by the antioxidant defense system, resulting in tissue damage. Madecassic acid (MA), an abundant triterpenoid in Centella asiatica (L.) Urban, has been used as a wound healing, antiinflammatory, and anticancer agent. Moreover, recent studies have shown that MA has an antioxidative effect, but the underlying mechanism remains unclear. Objective Here, we established an effective oxidative stress model induced by hydrogen peroxide (H 2 O 2 ) in human periodontal ligament fibroblasts (hPDLFs) to investigate the antioxidant and protective effects of MA against cell damage and its underlying mechanism of action. Results Pretreatment with MA inhibited cell apoptosis and promoted cell invasion and migration against oxidative injury induced by H 2 O 2 . In addition, MA was able to maintain mitochondrial membrane potential (ΔΨm) under oxidative stress. Notably, we found that MA restored redox balance by reducing intracellular ROS production. Furthermore, we investigated apoptosis-related proteins and found that the levels of anti-apoptosis markers Bcl-xL and Bcl-2 were remarkably upregulated, whereas that of the pro-apoptotic marker Bax was strikingly downregulated. Conclusions Collectively, these findings suggest that MA inhibits H 2 O 2 -induced oxidative stress and apoptosis of hPDLFs by reducing intracellular ROS production to maintain ΔΨm stability.