Role of anthocyanins in protecting chondrocytes from high glucose damage through SIRT-1 and autophagy in diabetic osteoarthritis
Issued Date
2025-12-01
Resource Type
ISSN
07533322
eISSN
19506007
Scopus ID
2-s2.0-105023970954
Journal Title
Biomedicine and Pharmacotherapy
Volume
193
Rights Holder(s)
SCOPUS
Bibliographic Citation
Biomedicine and Pharmacotherapy Vol.193 (2025)
Suggested Citation
Wudtiwai B., Sittiju P., Chongchai A., Udomruk S., Rujiphan A., Kongtawelert P., Phitak T., Pothacharoen P. Role of anthocyanins in protecting chondrocytes from high glucose damage through SIRT-1 and autophagy in diabetic osteoarthritis. Biomedicine and Pharmacotherapy Vol.193 (2025). doi:10.1016/j.biopha.2025.118870 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/113495
Title
Role of anthocyanins in protecting chondrocytes from high glucose damage through SIRT-1 and autophagy in diabetic osteoarthritis
Author's Affiliation
Corresponding Author(s)
Other Contributor(s)
Abstract
Diabetes mellitus is linked to osteoarthritis through high glucose (HG)-induced inflammation and chondrocyte apoptosis, causing cartilage degradation. Preventing these processes may mitigate diabetic osteoarthritis. This study evaluated the chondroprotective effects of anthocyanins from purple corn—cyanidin-3-O-glucoside (C3G), pelargonidin-3-O-glucoside (P3G), peonidin-3-O-glucoside (PLG)—and their metabolite protocatechuic acid (PCA) using HG-induced human chondrocyte and cartilage explant models. We assessed cytotoxicity, antioxidant activity, apoptosis, and signaling protein expression in C28I2 chondrocytes. All anthocyanins and PCA significantly reduced HG-induced apoptosis, associated with upregulation of SIRT-1 and p-AMPK pathways, indicating protective autophagy. Long-term HG exposure increased advanced glycation end products (AGEs) and glycosaminoglycan degradation in cartilage, which PCA effectively inhibited, correlating with reduced apoptosis. These findings suggest anthocyanins and PCA have therapeutic potential for diabetic osteoarthritis by protecting chondrocytes and cartilage from HG-induced damage.
