5-Bromo-3,4-dihydroxybenzaldehyde stabilizes diabetic retinal neurovascular units by inhibiting the inflammatory microenvironment

Background: Diabetic retinopathy (DR) is a leading cause of blindness characterized by damage to the retinal neurovascular unit, which is caused by hyperglycemia-induced metabolic and inflammatory responses. 5-Bromo3,4-dihydroxybenzaldehyde (BDB) is a compound derived from marine red algae and known for its antiinflammatory effects. Methods: This study aimed to investigate the potential protective effects of BDB on DR using primary human retinal vascular endothelial cells and retinal tissue explants. The analysis involved assessing vascular integrity, expression of tight junction protein, hyperglycemia-induced permeability, and retinal ganglion cell (RGC) apoptosis. The protective effect of BDB in maintaining the diabetic retinal neurovascular units was verified using type 1 diabetic mouse models. Additionally, the inhibitory effect of BDB on the levels of inflammatory cytokines TNF-alpha, IL-1 beta, and IL-6 were examined. Results: In vitro experiments revealed that BDB promoted vascular integrity, inhibited the transcription of proinflammatory factors, and alleviated hyperglycemia-induced permeability. BDB also protected RGC from hyperglycemia-induced apoptosis. In diabetic mice models, BDB treatment maintained the integrity of diabetic retinal neurovascular units and inhibited the secretion of TNF-alpha, IL-1 beta, and IL-6. Conclusion: BDB demonstrated a protective effect on DR by inhibiting the secretion of inflammatory factors, suggesting its potential as a therapeutic agent for the treatment of DR. Further research is warranted to validate its safety and efficacy for clinical application.

Automated summary

This study demonstrated that the compound 5-Bromo3,4-dihydroxybenzaldehyde (BDB) derived from marine red algae has a protective effect on diabetic retinopathy (DR). BDB promotes vascular integrity, inhibits the transcription of proinflammatory factors, alleviates hyperglycemia-induced permeability, and protects retinal ganglion cells (RGC) from hyperglycemia-induced apoptosis.