2. Academic Validation
  3. Diosmin ameliorates inflammation, apoptosis and activates PI3K/AKT pathway in Alzheimer's disease rats

Diosmin ameliorates inflammation, apoptosis and activates PI3K/AKT pathway in Alzheimer's disease rats

  • Metab Brain Dis. 2024 Aug 6. doi: 10.1007/s11011-024-01388-7.
Yanbo Wang 1,  Xiaojun Ye 2,  Wenwen Su 3,  Ci Yan 4,  Haiyan Pan 5,  Xiaowei Wang 6,  Sen Shao 7
Affiliations

Affiliations

  • 1 Department of Neurology, the Third Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, Zhejiang, 310000, China.
  • 2 Department of Neurology, the Affiliated Hospital of Hangzhou Normal University, Hangzhou, Zhejiang, 310015, China.
  • 3 Department of Internal Medicine, CiXi Seventh People's Hospital, Ningbo, Zhejiang, 315000, China.
  • 4 Departments of Psychiatry, Affiliated Mental Health Center, Zhejiang University School of Medicine, Hangzhou, Zhejiang, 310000, China.
  • 5 Department of Endocrinology, The Third Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, Zhejiang, 310000, China.
  • 6 Department of Respiratory Medicine, The Third Affiliated Hospital of Zhejiang Chinese Medicine University, Hangzhou, Zhejiang, 310000, China.
  • 7 Department of Neurology, Xixi Hospital of Hangzhou Affiliated to Zhejiang University School of Medicine, No. 2, Hengbu Street, Hangzhou, Zhejiang, 310023, China. hzsxxyy2015@sohu.com.
PMID: 39105973 DOI: 10.1007/s11011-024-01388-7
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.

Keywords

Alzheimer’s disease; Diosmin; PI3K/AKT signaling pathway; amyloid-β.

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