Cytoprotective mechanism of ferulic acid against high glucose-induced oxidative stress in
cardiomyocytes and hepatocytes
Sammanfattning
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 µg/mL FA), and a dimethylbiguanide (DMBG)+HG group (medium containing
80 mmol/L glucose and 50 µg/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.