Ginger (Zingiber Officinale Roscoe) ameliorates ethanol-induced cognitive impairment by modulating NMDA and GABA-A receptors in rat hippocampus.

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)-1ß 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-1ß pathway in the rat hippocampus.

Ginger (Zingiber officinale roscoe) extract could upregulate the renal expression of NRF2 and TNFα and prevents ethanol-induced toxicity in rat kidney.

OBJECTIVE: Ginger has protective effects on the kidney, however the molecular mechanism of this effect has not yet been fully elucidated. Therefore, this work studied molecular mechanisms of ginger effects on ethanol-induced kidney injury. MATERIALS AND METHODS: Twenty-four male Sprague-Dawley rats were randomly divided into four groups: control, ginger (1 g/kg/day ginger extract by oral gavage), ethanol (4 g/kg/day ethanol by oral gavage) and ginger-ethanol group and treated daily for 28 days. Kidney function, expression of nuclear factor erythroid 2-related factor 2 (NRF2) and tumor necrosis factor (TNF)-α genes and oxidative stress parameters in kidney tissue, were evaluated. Total phenolic content (TPC) and 2, 2-diphenyl-1-picrylhydrazyl (DPPH) scavenging activity of ginger extract were also evaluated. RESULTS: Hydroethanolic extract of ginger showed a good level of DPPH scavenging activity and TPC. In the ethanol group, serum level of urea, creatinine and uric acid and the expression of NRF2 and TNF-α significantly increased compared to control group, while co-treatment with ginger in ginger+ethanol group significantly ameliorated them compared to the ethanol group. Ethanol exposure significantly reduced the activity of superoxide dismutase  (SOD), glutathione peroxidase (GPx) and catalase (CAT) compared to the control values ,while the level of malondialdehyde (MDA) significantly increased. Ginger significantly ameliorated the level of MDA and activity of SOD, GPx and CAT in the ginger-ethanol group compared to the ethanol group. CONCLUSION: The results showed that ginger's protective effects against ethanol renotoxicity were mediated via enhancing the NRF2 and TNF-α expression.