Brain and behavior · 2025
Vitamin C and Gallic Acid Ameliorate Motor Dysfunction, Cognitive Deficits, and Brain Oxidative Stress in a Valproic Acid-Induced Model of Autism.
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Tarahomi Parnia, Arab Mina, Seyedinia Seyed Ali, Rahmani Mehrnoush, Rashidy-Pour Ali, Vafaei Abbas Ali, Raise-Abdullahi Payman
Аннотация
PURPOSE: Autism, a developmental-neurodegenerative disorder, often manifests as social communication difficulties and has been correlated to oxidative stress in the brain. Vitamins C and gallic acid (GA) possess potent antioxidant properties, making them potential candidates for addressing autism-related issues. This study examined the influence of vitamin C (Vit C) and GA on behavioral, motor, and cognitive performance, along with the assessment of brain oxidative markers, using an experimental model of autism.
METHOD: Fourteen female rats were divided into saline and valproic acid (VPA) groups, and mating with mature male rats generated offspring. VPA (500 mg/kg) was injected intraperitoneally (i.p.) on gestational day (GD) 12.5. Male pups remained undisturbed for 29 days. On postnatal day (PND) 30, 48 male pups were randomly selected and administered daily injections of Vit C (30 mg/kg, i.p.) or GA (30 mg/kg, i.p.) for 4 weeks (PND 38-65). Behavioral assessments were conducted before and after treatment (PND 30-37 and 66-73). Animals were then anesthetized, and their brains were analyzed for oxidative stress markers.
FINDING: The prenatal VPA-induced autism model increased nociceptive threshold, heightened anxiety-like behaviors, impaired balance power, delayed spatial learning, elevated malondialdehyde, and decreased glutathione and catalase levels in the brains of the male offspring. Administration of Vit C and GA effectively mitigated these anomalies.
CONCLUSIONS: Vit C and GA could potentially alleviate anxiety-like behaviors, motor and cognitive deficits, and brain oxidative stress markers in a prenatal rat autism model. This underscores their viability as potential pharmacological interventions for treating autistic dysfunction.
METHOD: Fourteen female rats were divided into saline and valproic acid (VPA) groups, and mating with mature male rats generated offspring. VPA (500 mg/kg) was injected intraperitoneally (i.p.) on gestational day (GD) 12.5. Male pups remained undisturbed for 29 days. On postnatal day (PND) 30, 48 male pups were randomly selected and administered daily injections of Vit C (30 mg/kg, i.p.) or GA (30 mg/kg, i.p.) for 4 weeks (PND 38-65). Behavioral assessments were conducted before and after treatment (PND 30-37 and 66-73). Animals were then anesthetized, and their brains were analyzed for oxidative stress markers.
FINDING: The prenatal VPA-induced autism model increased nociceptive threshold, heightened anxiety-like behaviors, impaired balance power, delayed spatial learning, elevated malondialdehyde, and decreased glutathione and catalase levels in the brains of the male offspring. Administration of Vit C and GA effectively mitigated these anomalies.
CONCLUSIONS: Vit C and GA could potentially alleviate anxiety-like behaviors, motor and cognitive deficits, and brain oxidative stress markers in a prenatal rat autism model. This underscores their viability as potential pharmacological interventions for treating autistic dysfunction.