BMC Ophthalmol. 2026 May 11. doi: 10.1186/s12886-026-04863-0. Online ahead of print.
ABSTRACT
BACKGROUND: Inflammation, oxidative stress, and apoptosis play important roles in diabetes-induced retinal injury. Coenzyme Q10 (CoQ10) is an endogenous antioxidant involved in mitochondrial energy metabolism and cellular protection. This study aimed to investigate the effects of CoQ10 on diabetes-induced retinal injury in a streptozotocin-induced diabetic rat model.
METHODS: Diabetes was induced in rats using streptozotocin. The animals were divided into 1- and 2-month experimental groups, each consisting of control, diabetic, CoQ10-treated, and diabetic + CoQ10 groups. CoQ10 was administered via oral gavage at a dose of approximately 30 mg/kg/day. Blood samples were collected for biochemical analysis, and retinal tissues were evaluated using immunohistochemical staining for tumor necrosis factor-alpha (TNF-α), nuclear factor kappa-B (NFκB), Bcl-2-associated X protein (Bax), vascular endothelial growth factor (VEGF), and VEGF receptor (VEGFR).
RESULTS: In the 2-month experimental group, SOD, GSH, and CAT levels were significantly higher in diabetic rats compared with the diabetic + CoQ10 group. Immunohistochemical analysis showed decreased staining intensities of VEGF, VEGFR, NFκB, and Bax in the diabetic + CoQ10 group compared with the diabetic group at the first month. In the second month, TNF-α, NFκB, and CD45 staining intensities were significantly reduced in the diabetic + CoQ10 group compared with the diabetic group.
CONCLUSION: These findings suggest that CoQ10 may modulate inflammatory, apoptotic, and oxidative stress pathways in diabetes-induced retinal injury. However, the protective effects appear to vary depending on the duration of diabetes. Further studies are required to clarify the potential role of CoQ10 in diabetic retinal disease.
PMID:42116018 | DOI:10.1186/s12886-026-04863-0