Neuroprotective Effects of Santonin on Aluminum Chloride-induced Oxidative Stress Mediated Neuroinflammation in Rat Model of Alzheimer’s Disease

Abstract

Alzheimer’s disease (AD) is one of the neurodegenerative diseases that is marked by deterioration in cognitive functioning and behavioral capacities in a progressive manner. It is the most prevalent cause of dementia in the aging population and imposes a high social and economic cost on the global population. In this study, we have examined Santonin, which can prevent the brain damage caused by aluminum chloride (AlCl 3 ) in rats, a typical method used to simulate the effects of AD in the laboratory. We administered AlCl 3 (100 mg/kg) to the rats to induce changes in them that resembled Alzheimer’s and tested their behavior using the open field and elevated plus maze tests. Then, we analyzed their brains in terms of the presence of inflammation, oxidative stress, enzyme activities, and tissue damage. The rats receiving AlCl 3 had reduced motility and an increase in acetylcholinesterase, malondialdehyde, and inflammatory cytokines, including cyclooxygenase-2, tumor necrosis factor-alpha, and interleukin-6. Their antioxidant defense mechanisms, glutathione, superoxide dismutase, and catalase, also decreased. However, these effects were changed positively when we treated rats with Santonin. Their movement was better, and they responded quicker, and their brains became less inflamed and less oxidatively stressed. Santonin reduced levels of harmful proteins and enzymes and restored antioxidant activity in a dose-dependent manner. Santonin helps reverse the brain changes and behavior problems caused by AlCl 3 in rats. It looks promising as a neuroprotective agent for AD.