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Diosmin ameliorates inflammation, apoptosis and activates PI3K/AKT pathway in Alzheimer's disease rats
Yanbo Wang1, Xiaojun Ye2, Wenwen Su3
1Department of Neurology, the Third Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, Zhejiang, 310000, China.
Abstract:
Alzheimer's disease (AD), a prevalent cognitive disorder among the elderly, is frequently linked to the abnormal accumulation of myloid-β (Aβ), which is mainly as a result of neuronal death and inflammation. Diosmin, a flavonoid, is considered a potential drug for the treatment of AD. Our study aimed to uncover the molecular mechanism of diosmin in AD therapy. Here, rats were randomly divided into three groups: control, Aβ25-35, and Aβ25-35 + diosmin groups. AD model rats were induced by Aβ25-35 intraventricular injection, meanwhile 50 mg/kg diosmin was orally administered for 6-week intervention. Morris water maze test assessed learning and memory abilities. Hippocampal neuronal damage was determined by HE, Nissl, and TUNEL staining. These assays indicate that diosmin improves cognitive dysfunction and reduces hippocampal neuronal loss and apoptosis. Western blot showed that diosmin reduced Bax (1.21 ± 0.12) and cleaved caspase-3 (1.27 ± 0.12) expression, and increased Bcl-2 (0.70 ± 0.06), p-PI3K (0.71 ± 0.08), and p-AKT (0.96 ± 0.10) in the hippocampus. ELISA indicated diosmin reduces IL-1β, IL-6, and TNF-α levels, suggesting anti-inflammation effect. These results suggest that diosmin inhibits neuronal apoptosis and neuroinflammatory responses to improve cognitive dysfunction in AD rats, possibly related to upregulation of the PI3K/AKT pathway, providing a scientific basis for its use in AD treatment.
Insights
Diosmin, a flavonoid, shows promise in treating Alzheimer's disease (AD) by improving cognitive function and reducing neuronal damage. This study reveals its anti-apoptotic and anti-inflammatory effects in an AD rat model.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Alzheimer's disease (AD) is a neurodegenerative disorder characterized by amyloid-beta (Aβ) accumulation, neuronal death, and inflammation.
- Current treatments for AD are limited, necessitating the exploration of novel therapeutic agents.
Purpose of the Study:
- To investigate the molecular mechanisms underlying the therapeutic effects of diosmin in an Alzheimer's disease rat model.
- To evaluate diosmin's impact on cognitive function, neuronal apoptosis, and neuroinflammation in AD.
Main Methods:
- An Alzheimer's disease rat model was induced using Aβ25-35 intraventricular injection.
- Rats were treated with diosmin (50 mg/kg) for 6 weeks, with cognitive function assessed via Morris water maze.
- Hippocampal neuronal damage, apoptosis, protein expression (Bax, Bcl-2, caspase-3, PI3K/AKT), and inflammatory cytokines (IL-1β, IL-6, TNF-α) were analyzed.
Main Results:
- Diosmin treatment significantly improved learning and memory in AD rats.
- Diosmin reduced hippocampal neuronal loss and apoptosis, decreasing Bax and cleaved caspase-3 while increasing Bcl-2 expression.
- Diosmin suppressed neuroinflammation by reducing IL-1β, IL-6, and TNF-α levels and upregulated the PI3K/AKT pathway.
Conclusions:
- Diosmin demonstrates neuroprotective effects in an AD rat model by inhibiting neuronal apoptosis and neuroinflammation.
- The findings suggest that diosmin's therapeutic potential in AD may be mediated through the upregulation of the PI3K/AKT signaling pathway.
- Diosmin represents a potential therapeutic candidate for Alzheimer's disease, warranting further clinical investigation.
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