Phenylethanoid Glycosides (AIE2)-Enriched Cistanche tubulosa Extract Attenuates Oxidative Stress and Amyloid Pathology in an Aβ1-40-Induced Rat Model of Alzheimer’s Disease
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-β (Aβ)-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 Aβ1-40-induced rat model. The AD-like model was established by hippocampal infusion of Aβ1-40. Antioxidant enzyme activities, including superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase, were evaluated. CTE treatment significantly attenuated Aβ1-40-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 Aβ1-40 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.
Cite this paper
Chou, C. , Chao, C. , Huang, W. , Wu, Y. , Huang, Y. , Lin, H. and Su, M. (2026). Phenylethanoid Glycosides (AIE2)-Enriched Cistanche tubulosa Extract Attenuates Oxidative Stress and Amyloid Pathology in an Aβ1-40-Induced Rat Model of Alzheimer’s Disease. Open Access Library Journal, 13, e14980. doi: http://dx.doi.org/10.4236/oalib.1114980.
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