High-Concentration Cyanidin-3-O-Glucoside Attenuates Palmitic Acid-Induced Oxidative Stress via ROS Suppression in Pancreatic β-Cells
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Issued Date
2026-01-01
Resource Type
eISSN
11791454
Scopus ID
2-s2.0-105039767425
Journal Title
Journal of Experimental Pharmacology
Volume
18
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SCOPUS
Bibliographic Citation
Journal of Experimental Pharmacology Vol.18 (2026)
Suggested Citation
Chitwattananont S., Sawasvirojwong S., Muanprasat C. High-Concentration Cyanidin-3-O-Glucoside Attenuates Palmitic Acid-Induced Oxidative Stress via ROS Suppression in Pancreatic β-Cells. Journal of Experimental Pharmacology Vol.18 (2026). doi:10.2147/JEP.S562755 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/117001
Title
High-Concentration Cyanidin-3-O-Glucoside Attenuates Palmitic Acid-Induced Oxidative Stress via ROS Suppression in Pancreatic β-Cells
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Abstract
Background: Type 2 diabetes mellitus (T2DM) is characterized by progressive β-cell dysfunction driven in part by palmitic acid (PA)-induced lipotoxicity. Cyanidin-3-O-glucoside (C3G) possesses antioxidant properties, but its temporal and mechanistic effects at higher concentrations remain poorly defined. Objective: This study aimed to investigate the continuous effects of high‑concentration of C3G on PA‑induced β‑cell apoptosis, with emphasis on time‑dependent efficacy and underlying antioxidant mechanisms. Methods: MIN6 cells were treated with PA (500 µM) in the presence or absence of C3G (500 µM). Cell viability was assessed by MTT assay, apoptosis by flow cytometry and cell death assay, oxidative stress by DCFDA and DPPH assays, and ER-stress related C/EBP homologous protein (CHOP) and apoptotic cleaved caspase-3 expression by Western blot analysis. Results: PA (500 µM) significantly reduced MIN6 cell viability, whereas continuous exposure to C3G (500 µM) restored viability, corresponding to a 40.9% increase (p < 0.001) compared with PA treatment alone. Flow cytometry showed that PA reduced live cells from 78.6% to 41.0% and increased early and late apoptotic populations to 27.7% and 28.2%, respectively, whereas C3G co-treatment reduced apoptosis to 17.7%. Consistently, cell death assays confirmed that C3G lowered apoptotic cells from 30.7% to 5.0% (p < 0.001 vs PA-treated groups) and restored viability to 93.1%, comparable to vehicle controls. Reactive oxygen species (ROS) assays, including DCFDA and DPPH, further demonstrated that C3G reduced PA‑induced ROS by 26.5% (p < 0.01 vs PA alone), consistent with free radical‑scavenging activity. Western blot analyses revealed that PA markedly upregulated CHOP and cleaved caspase‑3, which was suppressed by co‑treatment with C3G, confirming the attenuation by C3G of ER stress‑mediated apoptotic signaling. These findings imply that C3G rapidly counteracts oxidative stress-induced apoptosis. Conclusion: High-concentration C3G mitigates PA-induced oxidative stress and ER stress-associated apoptosis in β-cells, supporting its potential as a therapeutic agent for T2DM.