Brain damage caused by ethanol abuse may lead to permanent damage, including severe dementia. The aim of this study was to investigate the effects of ginger powder on ethanol-induced cognitive disorders by examining oxidative damage and inflammation status, and the gene expression of N-methyl-D-aspartate (NMDA) and γ-Aminobutyric acid (GABA)-A receptors in the hippocampus of male rats. 24 adult male Sprague–Dawley rats were allocated randomly to four groups as follows control, ethanol (4g/kg/day, by gavage), ginger (1g/kg/day, by gavage), and ginger-ethanol. At the end of the study, memory and learning were evaluated by the shuttle box test. Moreover, to explore mechanisms involved in ethanol-induced cognitive impairment and the protective effect of ginger, the expression of Nuclear factor kappa B (NF-κB), nuclear factor erythroid 2–related factor 2 (Nrf2), NMDA receptor, and GABA-A receptor was measured along with inflammatory and oxidative biomarkers in the hippocampus tissue. The results showed that ethanol could induce cognitive impairment in the ethanol group, while pretreatment with ginger could reverse it. The gene expression of the NF-κB/ Tumor necrosis factor (TNF)-α/Interleukin (IL)-1β pathway and NMDA and GABA-A receptors significantly increased in the ethanol group compared to the control group. While pretreatment with ginger could significantly improve ethanol-induced cognitive impairment through these pathways in the ginger-ethanol group compared to the ethanol group (P < 0.05). It can be concluded that ginger powder could ameliorate ethanol-induced cognitive impairment by modulating the expression of NMDA and GABA-A receptors and inhibiting oxidative damage and the NF-κB/TNF-α/IL-1β pathway in the rat hippocampus.

滥用乙醇造成的脑损伤可能会导致永久性损伤，包括严重的痴呆症。本研究的目的是通过检查氧化损伤和炎症状态以及 N-甲基-D-天冬氨酸 (NMDA) 和 γ-氨基丁酸 (GABA) 的基因表达来研究生姜粉对乙醇引起的认知障碍的影响雄性大鼠海马体中的 -A 受体。24只成年雄性Sprague-Dawley大鼠随机分为四组，分别为对照组、乙醇组（4g/kg/天，灌胃）、姜组（1g/kg/天，灌胃）和姜-乙醇组。研究结束时，通过穿梭箱测试评估记忆和学习能力。此外，为了探讨乙醇引起的认知障碍的机制以及生姜的保护作用，研究了核因子κB (NF-κB)、核因子红细胞2相关因子2 (Nrf2)、NMDA受体和GABA的表达。对海马组织中的受体以及炎症和氧化生物标志物进行了测量。结果表明，乙醇会引起乙醇组的认知障碍，而生姜预处理可以逆转这种情况。与对照组相比，乙醇组中 NF-κB/肿瘤坏死因子 (TNF)-α/白细胞介素 (IL)-1β 通路以及 NMDA 和 GABA-A 受体的基因表达显着增加。而生姜预处理可通过这些途径显着改善生姜-乙醇组与乙醇组相比乙醇引起的认知障碍（P  < 0.05）。由此可见，生姜粉可通过调节大鼠海马NMDA和GABA-A受体的表达、抑制氧化损伤和NF-κB/TNF-α/IL-1β通路来改善乙醇引起的认知障碍。