Zingiber officinale protects against acrylamide-induced spatial memory impairment, oxidative stress, and neurodegeneration in rats

Moradi, Hamid Reza; Khaksar, Zabihollah; Alipour, Fatemeh; Fathollahi, Saeid; Taherianfard, Mahnaz; Rashidi, Mohsen; Khodayari, Melika

doi:10.22038/ajp.2026.27806

Zingiber officinale protects against acrylamide-induced spatial memory impairment, oxidative stress, and neurodegeneration in rats

Articles in Press

Document Type : Original Research Article

Authors

Department of Basic Sciences, School of Veterinary Medicine, Shiraz University, Shiraz, Iran

10.22038/ajp.2026.27806

Abstract

Objective: Acrylamide (ACA), an environmental and dietary contaminant, induces oxidative stress, neuroinflammation, and apoptosis, leading to cognitive impairment. This study investigated the neuroprotective potential of ginger (Zingiber officinale) hydroalcoholic extract (ZOE) against chronic ACA-induced neurotoxicity in rats.
Materials and methods: Thirty-two male Sprague-Dawley rats (n = 8 per group) were randomly assigned to four groups, each receiving a daily oral gavage for 52 days: healthy control (1 ml distilled water), ACA (10 mg/kg/day), ZOE (200 mg/kg/day), and ACA+ZOE )10 + 200 mg/kg/day). Spatial learning and memory were evaluated using the Morris water maze (MWM). Oxidative stress indices including total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI), as well as histomorphometric parameters and immunohistochemical (IHC) markers of apoptosis and gliosis (p53, Bcl-2, and GFAP) were assessed in the hippocampus and parietal cortex. Data were analyzed using one-way and two-way ANOVA, followed by Tukey’s post hoc test.
Results: ACA exposure led to spatial memory acquisition impairment, accompanied by increased TOS and OSI, reduced TAC, decreased neuronal density and layer thickness, and upregulation of p53 and GFAP, and downregulation of Bcl-2 expression. ZOE co-administration markedly mitigated these effects by preserving neuronal architecture, restoring redox balance, and normalizing apoptosis- and gliosis-related protein expression.
Conclusion: Overall, our findings provide integrated behavioral, biochemical, histological, and molecular evidence supporting ZOE as a promising therapeutic candidate for environmentally induced neurotoxicity.

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