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Raddeanin A Protects the BRB Through Inhibiting Inflammation and Apoptosis in the Retina of Alzheimer's Disease
Xiao-Fang Wang1,2, Xiao-Hong Xiang3, Jing Wei4
1Laboratory Animal Centre, Model Animal and Human Disease Research of Luzhou Key Laboratory, Southwest Medical University, Luzhou, China.
Abstract:
Neuroinflammation and endothelial cell apoptosis are prominent features of blood-brain barrier (BBB) disruption, which have been described in Alzheimer's disease (AD) and can predict cognitive decline. Recent reports revealed vascular β-amyloid (Aβ) deposits, Muller cell degeneration and microglial dysfunction in the retina of AD patients. However, there has been no in-depth research on the roles of inflammation, retinal endothelial cell apoptosis, and blood-retinal barrier (BRB) damage in AD retinopathy. We found that Raddeanin A (RDA) could improve pathological and cognitive deficits in a mouse model of Alzheimer's disease by targeting β-amyloidosis, However, the effects of RDA on AD retinal function require further study. To clarify whether RDA inhibits inflammation and apoptosis and thus improves BRB function in AD-related retinopathy. In vitro we used Aβ-treated HRECs and MIO-M1 cells, and in vivo we used 3×Tg-AD mice to investigate the effect of RDA on BRB in AD-related retinopathy. We found that RDA could improve BRB function in AD-related retinopathy by inhibiting NLRP3-mediated inflammation and suppressing Wnt/β-catenin pathway-mediated apoptosis, which is expected to improve the pathological changes in AD-related retinopathy and the quality of life of AD patients.
Insights
Raddeanin A (RDA) improves Alzheimer's disease (AD) retinopathy by reducing inflammation and cell death. This treatment protects the blood-retinal barrier (BRB), offering potential benefits for AD patients.
Area of Science:
- Neuroscience
- Ophthalmology
- Pharmacology
Background:
- Alzheimer's disease (AD) is linked to blood-brain barrier (BBB) disruption, neuroinflammation, and endothelial cell apoptosis.
- Retinal changes, including vascular amyloid-beta (Aβ) deposits and microglial dysfunction, are observed in AD patients.
- The specific roles of inflammation, endothelial cell apoptosis, and blood-retinal barrier (BRB) damage in AD retinopathy remain under-investigated.
Purpose of the Study:
- To investigate the therapeutic effects of Raddeanin A (RDA) on AD-related retinopathy.
- To determine if RDA can inhibit inflammation and apoptosis, thereby improving BRB function in AD retinopathy.
- To elucidate the underlying mechanisms of RDA's action on the BRB in AD.
Main Methods:
- In vitro studies using Aβ-treated human retinal endothelial cells (HRECs) and MIO-M1 cells.
- In vivo studies utilizing the 3×Tg-AD mouse model of Alzheimer's disease.
- Assessment of BRB function, inflammation (NLRP3 inflammasome), and apoptosis (Wnt/β-catenin pathway) following RDA treatment.
Main Results:
- RDA treatment improved BRB function in the 3×Tg-AD mouse model.
- RDA inhibited NLRP3 inflammasome-mediated inflammation in the retina.
- RDA suppressed Wnt/β-catenin pathway-mediated apoptosis in retinal cells.
Conclusions:
- Raddeanin A (RDA) effectively improves blood-retinal barrier (BRB) function in a mouse model of Alzheimer's disease (AD) retinopathy.
- RDA exerts its protective effects by inhibiting NLRP3-mediated inflammation and Wnt/β-catenin pathway-driven apoptosis.
- These findings suggest RDA holds promise for treating AD-related retinopathy and improving patients' quality of life.
