Mechanism of Melatonin on Inhibition of Inflammation and Apoptosis in Rats with Diabetic Retinopathy

Background Diabetic retinopathy (DR) is a severe microvascular complication of diabetes and a leading cause of vision impairment worldwide, with inflammation and apoptosis playing crucial roles in its pathogenesis. Purpose Based on a rat model of DR, the therapeutic effects of melatonin and a specific inhibitor on retinal lesions were compared, and their molecular mechanisms were explored. Materials and Methods We carefully selected 48 rats for the experiment. They will be evenly divided into four groups for the experiment: normal, inhibitor, model, and melatonin. The model, inhibitor, and melatonin groups underwent retinal lesion induction. After modeling, the model group received normal saline, the inhibitor group received SB 203580, and the melatonin group received melatonin. After 7 days, samples were collected for analysis. Western blotting was used to measure the protein expression levels of caspase-3, P38 mitogen-activated protein kinase (p38 MAPK), and phosphorylated P38 mitogen-activated protein kinase (p-p38 MAPK). The normal group served as an untreated control. Quantitative polymerase chain reaction (qPCR) was performed to detect Bcl-2-associated X protein (Bax) and B-cell lymphoma 2 (Bcl-2) messenger ribonucleic acid (mRNA) expression, and enzyme-linked immunosorbent assay (ELISA) was used to measure serum interleukin-1 beta (IL-1β) and interleukin-18 (IL-18) levels. Results Western blot analysis revealed no significant differences in the expression levels of p38 MAPK protein across all experimental groups ( p > .05). However, the levels of phosphorylated p38 MAPK (P-p38 MAPK) and caspase-3 were significantly higher in the model, melatonin, and inhibitor groups compared to the normal group ( p < .05). In contrast, these levels were reduced considerably in the melatonin and inhibitor groups relative to the model group ( p < .05). qPCR analysis showed significant upregulation of Bax mRNA and downregulation of Bcl-2 mRNA in the model, melatonin, and inhibitor groups compared to the normal group ( p < .05). After treatment, both the melatonin and inhibitor groups exhibited significant decreases in Bax expression and increases in Bcl-2 expression compared to the model group ( p < .05). ELISA results indicated significantly higher levels of IL-1β and IL-18 in the model, melatonin, and inhibitor groups compared to the normal group ( p < .05). Compared to the model group, both the melatonin and inhibitor groups showed significant reductions in IL-1β and IL-18 levels ( p < .05). Conclusion Melatonin can suppress inflammation and apoptosis in DR rats by modulating the MAPK signaling pathway.