Neuroprotective Effects of Tephrosin on Aluminium Chloride-induced Oxidative Stress Mediated Neuroinflammation in Rat Model of Alzheimer's Disease

Indian Journal of Pharmaceutical Education and Research

  • Hongxing Xue1Hunan University of Chinese Medicine, Bachelor’s Road, Hanpu Science and Education Park, Yuelu, Changsha City, Hunan Province, CHINA.
  • Weijuan Nan2Thoracic and Cardiac Surgery, General Hospital of Ningxia Medical University, Shengli Street, Xingqing, Yinchuan City, Ningxia Hui Autonomous Region, CHINA.
  • Qiang Li3Department of Brain Diseases, Zhongwei Traditional Chinese Medicine Hospital, West of Ninggang Avenue and Intersection of Huifeng Road and Feng’an Road, Shapotou District, Zhongwei City, Ningxia Hui Autonomous Region, CHINA.

Volume 60 Issue 4 Pages 1696-1705

DOI: 10.5530/ijper.20262570

Abstract

Aim/Background: Alzheimer’s Disease (AD) is a progressive neurodegenerative disorder with limited therapeutic options. Tephrosin (TP), a natural rotenoid, exhibits antioxidant and anti-inflammatory properties. This study investigated the neuroprotective effects of TP in an Aluminum Chloride (AlCl₃)-induced rat model of Alzheimer-like pathology. Materials and Methods: Twenty-four adult rats were divided into four groups (n=6): Control, AlCl₃, AlCl₃ + TP, and AlCl₃ + Donepezil. AD-like symptoms were induced by oral AlCl₃ (100 mg/kg) for six weeks. TP (10 mg/kg) or Donepezil (1 mg/kg) was administered orally during the last three weeks. Behavioral performance was evaluated using the wire hang and beam walking tests. Acetylcholinesterase (AChE) activity, oxidative stress markers [Malondialdehyde (MDA), Glutathione (GSH), Catalase (CAT), Superoxide Dismutase (SOD)], and pro-inflammatory cytokines [Interleukin-1β (IL-1β), Tumor Necrosis Factor-α (TNF-α)] were measured. Hippocampal histology was assessed using hematoxylin and eosin staining. Results: AlCl₃ exposure impaired motor function, increased MDA and AChE activity, elevated IL-1β and TNF-α levels, and caused hippocampal neuronal degeneration, while reducing GSH, CAT, and SOD activities. TP treatment significantly improved behavioral outcomes, restored antioxidant enzyme levels, reduced oxidative stress and inflammatory markers, and preserved hippocampal neuronal integrity. Conclusion: Tephrosin exerts neuroprotective effects against AlCl₃-induced Alzheimer-like pathology, likely via its antioxidant, anti-inflammatory, and anti-cholinesterase activities. These findings support TP as a promising candidate for AD therapy.

Keywords

  • AlCl3
  • Alzheimer's Disease
  • Tephrosin
  • Oxidative Stress
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