Neuroprotective Role of Periplocin Against Aluminium Chloride-stimulated Alzheimer’s Disease in a Rat Model by Modulation of Oxidative Stress and Inflammation

Abstract:

Background: Alzheimer’s disease is a prevalent neurodegenerative condition marked by the assembly of ß-amyloid deposits inside the brain parenchyma. Aluminium is a neurotoxin molecule that generates oxidative stress linked to various neurological disorders. Objectives: This study focused on the neuroprotective effects of periplocin, a natural compound, against aluminium chloride (AlCl₃)-stimulated diseased rat model. Materials and Methods: Four groups of twenty-four Sprague Dawley rats were established. For four weeks, the rats in the control group I was administered NaCl. AlCl₃ was provided to the second group of rats. An hour before AlCl₃ induction, rats in groups III and IV were given periplocin (25 and 50 mg/kg) orally. The rats were behaviourally examined before euthanization and analysis of the biochemical parameters was carried out after their sacrifice. Results: The learning ability and memory were impaired, lipid oxidation (MDA) was suppressed by antioxidant regulation (Reduced glutathione, Catalase, and Superoxide dismutase), and lactate dehydrogenase, Na⁺ K⁺ ATPase, acetylcholinesterase, and nitric oxide activity was inhibited upon periplocin administration. Additionally, the concentrations of inflammatory regulators such as Il-1β, TNF-α, and IL-6 were suppressed. Conclusion: Thus, periplocin might be a crucial neuroprotector against the advancement of Alzheimer’s disease.

Keywords: Periplocin, Alzheimer’s disease, Aluminium chloride, Neuroinflammation, Acetylcholinesterase.