The mechanisms underlying accelerated cognitive decline in Alzheimer¡¯s disease (AD) remain incompletely understood. Accumulating evidence suggests that AD is a complex, multifactorial neurodegenerative disorder in which oxidative stress plays a central role. Oxidative stress, often triggered by amyloid-¦Â (A¦Â)-induced reactive oxygen species (ROS), leads to severe cellular damage and contributes to cognitive deterioration. This study investigated the effects of phenylethanoid glycosides (AIE2)-enriched Cistanche tubulosa extract (CTE) on oxidative stress, cognitive impairment, and AD-like pathology in an A¦Â1-40-induced rat model. The AD-like model was established by hippocampal infusion of A¦Â1-40. Antioxidant enzyme activities, including superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase, were evaluated. CTE treatment significantly attenuated A¦Â1-40-induced oxidative stress, enhanced antioxidant enzyme activities, and improved cognitive performance in the AD-like animal model. Toxicological evaluation revealed no adverse effects, as evidenced by stable body weight and unchanged liver and kidney function parameters. Additionally, CTE reduced acetylcholinesterase activity as well as A¦Â1-40 and apolipoprotein E deposition without inducing toxicity. These findings suggest that CTE exerts antioxidant and neuroprotective effects and may represent a promising therapeutic candidate for the treatment of Alzheimer¡¯s disease.
%K Cistanche tubulosa %K Phenylethanoid Glycosides %K Alzheimer¡¯s Disease %K Oxidative Stress %K A¦Â1-40 %U http://www.oalib.com/paper/6889191