Neuroprotective effects of ononin against the aluminium chloride-induced Alzheimer’s disease in rats

Abstract

Alzheimer’s disease (AD) is a chronic neurodegenerative disease categorized by the deficiency in the cognition and memory. Approximately 50 million peoples has the AD, which is categorized by the deficiency in the cognition, memory and other kinds of cognitive dissention. The present exploration was designed to unveil the ameliorative properties of ononin against the aluminium chloride (AlCl3)-provoked AD in animals via the suppression of oxidative stress and neuroinflammation. AD was provoked to the Sprague Dawley rats through administering orally with 0.5 ml/100 g b.wt. of AlCl3 25 days and then supplemented with the 30 mg/kg of ononin orally for 25th day to 36th day. The behavioural changes were examined using open field and Morris Water Maze test. The acetylcholine esterase (AChE) activity was studied by standard method. The status of Aβ1-42, MDA, SOD, total antioxidant capacity (TAC) were quantified using respective assay kits. The interleukin(IL)-1β and TNF-α, BDNF, PPAR-γ, p38MAPK, and NF-κB/p65 status was quantified using respective assay kits. Brain histology was studied using microscope. The ononin treatment effectively modulated the AlCl3-triggered behavioural alterations in the AD animals. Ononin appreciably suppressed the AChE, Aβ1-42, and MDA and improved the SOD and TAC in the brain tissues of AD animals. The status of IL-1β, TNF-α, p38MAPK, and NF-κB were suppressed and the BDNF and PPAR-γ contents were elevated in the brain tissues of AD animals. The outcomes brain histology analysis proved the attenuate role of ononin. Our findings recommended that the ononin treatment could ameliorate the cognitive impairment, suppress the neuroinflammation and oxidative stress in the AD animals.

Keywords

• Ononin
• Neuroinflammation
• Alzheimer’s disease
• Oxidative stress
• PPAR-γ