摘要
Despite the recognized neuroprotective benefits of curcumin, its clinical utility is constrained by poor bioavailability and high cytotoxicity at effective doses. This study evaluates the therapeutic potential of curcumin-derived carbon quantum dots (Cur-CQDs) for retinal protection against ischemia-reperfusion (IR) injury in rats. Cur-CQDs were synthesized
mild pyrolysis at varying temperatures and assessed for efficacy in rat retinal ganglion cells and a model of retinal IR injury. The Cur-CQDs, particularly those synthesized at 150 °C, displayed significant reductions in apoptosis in retinal tissues, as indicated by TUNEL assays, immunofluorescence localization of HIF-α, CD68, BCL-2, and Grp78, and Western blot analysis for HO-1, Grp78, CHOP, caspase 3, and Nrf2. These results suggest that Cur-CQDs not only enhance cell survival and reduce inflammation but also decrease oxidative and endoplasmic reticulum stress markers. Mechanistic insights reveal that Cur-CQDs modulate pathways involved in oxidative stress, apoptosis, and inflammation, specifically through the upregulation of BCL-2 and HO-1 and the downregulation of CHOP, caspase-3, and endoplasmic reticulum stress markers. The identification of cinnamic acid-, anisole-, guaiacol, and ferulic acid-like structures on Cur-CQDs' surfaces may contribute to their superior antioxidative and anti-inflammatory activities. Collectively, these findings position Cur-CQDs as a promising approach for treating retinal IR injuries, enhancing curcumin's bioavailability and therapeutic efficacy, and paving new pathways in ocular neuroprotection research and potential clinical applications.