Albiflorin alleviates cognitive dysfunction in STZ-induced rats.
Xiaojun Ma1, Min Song1, Yushan Yan1
1Department of Endocrinology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, Henan, China.
Aging
|July 28, 2021
Summary
Albiflorin (AL) treatment improved cognitive function and reduced amyloid-beta plaques in rats with streptozotocin-induced Alzheimer's disease (AD). AL also regulated oxidative stress and inflammation, suggesting therapeutic potential for AD.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Alzheimer's disease (AD) is a neurodegenerative disorder characterized by cognitive decline.
- Streptozotocin (STZ) is used to induce an AD-like model in rodents.
- Investigating natural compounds for AD treatment is crucial.
Purpose of the Study:
- To investigate the therapeutic effects of albiflorin (AL) on STZ-induced AD in a rat model.
- To explore the underlying mechanisms of AL's action, including its impact on oxidative stress and inflammation.
Main Methods:
- A rat model of STZ-induced AD was established.
- Cognitive function was assessed using the step-down and Morris water maze tests.
- Amyloid-beta (Aβ) plaque distribution, serum insulin, glucose tolerance, oxidative stress markers (SOD, MDA), and hippocampal signaling pathways (Nrf-2/HO-1/HMGB1/NF-kB) were analyzed.
Main Results:
- AL treatment significantly improved cognitive function in STZ-induced AD rats.
- AL reduced Aβ plaque density in the hippocampus.
- AL modulated serum insulin, improved glucose tolerance, and regulated the Nrf-2/HO-1/HMGB1/NF-kB pathway, indicating reduced oxidative stress and inflammation.
Conclusions:
- Albiflorin demonstrates significant neuroprotective effects against STZ-induced Alzheimer's disease in rats.
- AL ameliorates cognitive impairment by mitigating amyloid-beta deposition, oxidative stress, and neuroinflammation.
- AL shows promise as a potential therapeutic agent for Alzheimer's disease.
