Journal of studies on alcohol and drugs · 2026
Coenzyme Q10 Mitigates Anxiety- and Depression-Like Behaviors in a Fetal Alcohol Spectrum Disorder Model by Suppressing Hippocampal Astrocytic Reactivity, Oxidative Stress, and Neuronal Cell Death.
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Adabi Razieh, Mohseni Fahimeh, Masoudi Alireza, Rafaiee Raheleh
Аннотация
OBJECTIVE: Fetal alcohol spectrum disorder (FASD) results from prenatal alcohol exposure and is associated with long-term neurobehavioral deficits, including anxiety and depression. Ethanol-induced oxidative stress, neuroinflammation, and hippocampal damage are key contributors to these outcomes. Coenzyme Q10 (CoQ10), a mitochondrial antioxidant, may offer neuroprotection against such ethanol-induced damage. This study aimed to investigate the potential therapeutic effects of CoQ10 on anxiety- and depression-like behaviors and hippocampal neurotoxicity in a neonatal rat model of FASD.
METHOD: Neonatal Wistar rats were exposed to ethanol (5.25 g/kg/day) via oral gavage from postnatal day (PD) 2 to PD10 (corresponding to the third trimester of human brain development). CoQ10 (30 mg/kg, intraperitoneal [i.p.]) was administered daily after ethanol exposure. Behavioral testing was performed on PD38-39 using the Elevated Plus Maze (EPM) and Forced Swim Test (FST). On PD40, biochemical assays measured malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Immunohistochemistry assessed glial fibrillary acidic protein (GFAP) and cleaved caspase-3 expression, and Nissl staining evaluated necrotic cell death in the CA1 hippocampal region.
RESULTS: CoQ10 significantly improved anxiety- and depression-like behaviors in ethanol-exposed rats (EPM: p = .0001-.0099; FST: p = .0021). It markedly reduced MDA levels (p = .0010) to near-control values (p = .4614, N.S.) and partially restored antioxidant enzyme activities (SOD: p = .0112 vs. control p = .0108; GSH: p = .0092 vs. control p = .3643, N.S.; CAT: p = .0003 vs. control p = .0769, N.S.). CoQ10 largely normalized astrocytic activation (GFAP: ethanol vs. CoQ10 p < .0001; CoQ10 vs. control p = .0196) and reduced cleaved caspase-3 expression (ethanol vs. CoQ10 p = .0407; CoQ10 vs. control p = .8940, N.S.). Furthermore, CoQ10 significantly decreased hippocampal necrotic cell death (ethanol vs. CoQ10 p = .0074), although a difference persisted versus controls (p < .0001).
CONCLUSIONS: CoQ10 administration mitigates behavioral and cellular manifestations of FASD by counteracting oxidative stress, astrocytic reactivity, and neuronal apoptosis/necrosis, thereby contributing to hippocampal functional recovery.
METHOD: Neonatal Wistar rats were exposed to ethanol (5.25 g/kg/day) via oral gavage from postnatal day (PD) 2 to PD10 (corresponding to the third trimester of human brain development). CoQ10 (30 mg/kg, intraperitoneal [i.p.]) was administered daily after ethanol exposure. Behavioral testing was performed on PD38-39 using the Elevated Plus Maze (EPM) and Forced Swim Test (FST). On PD40, biochemical assays measured malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione (GSH). Immunohistochemistry assessed glial fibrillary acidic protein (GFAP) and cleaved caspase-3 expression, and Nissl staining evaluated necrotic cell death in the CA1 hippocampal region.
RESULTS: CoQ10 significantly improved anxiety- and depression-like behaviors in ethanol-exposed rats (EPM: p = .0001-.0099; FST: p = .0021). It markedly reduced MDA levels (p = .0010) to near-control values (p = .4614, N.S.) and partially restored antioxidant enzyme activities (SOD: p = .0112 vs. control p = .0108; GSH: p = .0092 vs. control p = .3643, N.S.; CAT: p = .0003 vs. control p = .0769, N.S.). CoQ10 largely normalized astrocytic activation (GFAP: ethanol vs. CoQ10 p < .0001; CoQ10 vs. control p = .0196) and reduced cleaved caspase-3 expression (ethanol vs. CoQ10 p = .0407; CoQ10 vs. control p = .8940, N.S.). Furthermore, CoQ10 significantly decreased hippocampal necrotic cell death (ethanol vs. CoQ10 p = .0074), although a difference persisted versus controls (p < .0001).
CONCLUSIONS: CoQ10 administration mitigates behavioral and cellular manifestations of FASD by counteracting oxidative stress, astrocytic reactivity, and neuronal apoptosis/necrosis, thereby contributing to hippocampal functional recovery.