Cytoprotective mechanism of ferulic acid against high glucose-induced oxidative stress in cardiomyocytes and hepatocytes

卷:60

Song, Yuan ; Wen, Luona ; Sun, Jianxia ; Bai, Weibin ; Jiao, Rui ; Hu, Yunfeng ; Peng, Xichun ; He, Yong ; Ou, Shiyi

Jinan Univ

关键词: ferulic acid;    oxidative stress;    cardiomyocytes;    hepatocytes;   

DOI  :  10.3402/fnr.v60.30323

学科分类：食品科学和技术

【 摘 要 】

Background: Ferulic acid (FA), a phenolic acid, is a potential therapy for diabetes mellitus. FA has been shown to protect against hepatic and myocardial injury and oxidative stress in obese rats with late-stage diabetes, but the mechanism of the antioxidative activity of FA is still unclear. Objective: The aim of this study was to elucidate whether FA can prevent damage to cardiomyocytes and hepatocytes caused by high glucose (HG)-induced oxidative stress and whether the protection effects of FA on these cells are related to the Keap1-Nrf2-ARE signaling pathways. Design: Cells were divided into four groups: a control group (cultured with normal medium), an HG group (medium containing 80 mmol/L glucose), an FA + HG group (medium containing 80 mmol/L glucose and 1, 5, or 10 mu g/mL FA), and a dimethylbiguanide (DMBG) + HG group (medium containing 80 mmol/L glucose and 50 mu g/mL DMBG). Results: FA treatment significantly increased cell viability and significantly decreased cell apoptosis compared with the HG-treated group. Moreover, FA down-regulated the expression of Keap1 protein and up-regulated the expression of Nrf2 protein and gene transcription of HO-1 and glutathione S-transferase (GST) in a dose-dependent manner. Conclusion: FA alleviated the HG-induced oxidative stress and decreased cell apoptosis in hepatocytes and cardiomyocytes. These effects were associated with the Keap1-Nrf2-ARE signaling pathway.