Ameliorating Effects of Aloe Emodin in an Aluminum-Induced Alzheimer’s Disease Rat Model

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disease and threatens the health of the aged population worldwide. In the present study, we investigated cognitive improvement by aloe emodin in aluminum-induced AD rats. We orally administered aluminum chloride (150 mg/kg) to Sprague–Dawley rats for 8 weeks to induce AD. In the 5th to the 8th week, the rats were injected intraperitoneally with AE (5, 10, and 15 mg/kg). Behavioral, histopathological, and biochemical assessments were performed. The results showed that AE alleviated cognitive impairment in aluminum-induced AD rats and inhibited aluminum-induced hippocampal neuronal damage. Furthermore, aloe emodin relieved the aluminum burden in the brain of aluminum-induced AD rats, attenuated the aluminum-induced increase in Aβ₄₂ level and acetylcholinesterase activity, and reduced the levels of tumor necrosis factor-α, interleukin-6, interleukin-1α, and interleukin-1β. These effects suggest that the mechanism by which AE alleviates AD-related cognitive impairment is by removal of excess aluminum, decreasing Aβ₄₂ deposition, regulating the cholinergic system, and reducing neuroinflammation.