Huangqi Gegen decoction ameliorates alcohol-induced cognitive dysfunction via attenuating oxidative stress and enhancing blood-brain barrier integrity in rats through the Keap1-Nrf2/HO-1 signaling pathway | ||
| Iranian Journal of Basic Medical Sciences | ||
| مقاله 14، دوره 27، شماره 10، دی 2024، صفحه 1331-1339 اصل مقاله (1.15 M) | ||
| نوع مقاله: Original Article | ||
| شناسه دیجیتال (DOI): 10.22038/ijbms.2024.77415.16737 | ||
| نویسندگان | ||
| Yang Qiao1؛ Qing Yuan* 2؛ Zhen Liu* 1 | ||
| 1Department of Traditional Chinese Medicine, Baotou Central Hospital, Baotou, Inner Mongolia, China | ||
| 2State Key Laboratory of Component-based Chinese Medicine, Tianjin Key Laboratory of Traditional Chinese Medicine Pharmacology, Tianjin University of Traditional Chinese Medicine, Tianjin, China | ||
| چکیده | ||
| Objective(s): Chronic alcohol abuse causes cognitive deficits. Huangqi Gegen Decoction (HGD), a traditional Chinese herbal formula comprising Huangqi and Gegen, has been documented for its therapeutic efficacy in the treatment of alcoholic liver injury. However, its potential neuroprotective effects against alcohol-induced brain injury remain unexplored. This study aims to evaluate the neuroprotection of HGD on alcohol-induced cognitive dysfunction and the associated mechanism. Materials and Methods: Wistar rats were orally administered 50% ethanol for 10 weeks, followed by treatment with HGD at doses of 16, 32, or 64 mg/kg/day for an additional 6 weeks. The spatial learning and memory abilities of rats were assessed through the Morris Water Maze experiment. The pathological condition in the hippocampus was assessed using H&E and Nissl staining. Tight junction proteins, oxidative stress, and inflammation cytokines were measured by IF, ELISA, PCR, and western blot. The mRNA and protein expression of Keap1, Nrf-2, HO-1, and NQO-1 were tested by PCR and western blot. Results: Results showed that HGD effectively mitigated cognitive dysfunction and pathological changes in alcohol-induced rats while enhancing the expression of ZO-1, Occludin, and Claudin-5. Furthermore, HGD effectively mitigated oxidative stress by reducing levels of ROS and MDA, while elevating levels of SOD, CAT, and GSH-PX in brain tissue. Moreover, HGD significantly suppressed microglial activation and down-regulated expressions of IL-1β, IL-6, and TNF-α. Mechanistically, HGD remarkably up-regulated the expression of Nrf-2, HO-1, and NQO-1 while down-regulating Keap1 expression. Conclusion: These findings suggest that HGD may be a promising therapeutic agent for alleviating alcohol-induced cognitive dysfunction. | ||
| کلیدواژهها | ||
| Alcohols؛ Blood-Brain Barrier؛ Cognitive dysfunction HuangQi؛ Oxidative stress؛ Pueraria | ||
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