ArticleIranian journal of basic medical sciences2026
Promising therapeutic efficacy of kolaviron against prenatal valproate-induced autism spectrum disorder.
Article in Iranian journal of basic medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objectives: Autism spectrum disorder (ASD) is a lifelong neurodevelopmental condition marked by impairments in social communication, language, and behavior. Prenatal exposure to valproic acid (VPA) contributes to its pathogenesis. kolaviron (KV), a polyphenolic extract from Garcinia kola, has potent antioxidant and anti-inflammatory properties, offering neuroprotective potential in ASD models. Our study aimed to evaluate whether KV could improve the VPA-induced autism model through targeting serotonergic system, mitochondrial dysregulation, oxidative stress, and inflammation. Materials and Methods: Pregnant Wistar rats received a single intraperitoneal dose of VPA (600 mg/kg) on gestational day 12.5 to induce autism-like features in offspring. Male pups were weaned on postnatal day (PND) 21 and randomly assigned to receive KV (50 or 100 mg/kg, oral), or saline until PND 49. Behavioral tests were finally conducted and brain tissue was collected for analysis of hippocampal oxidative stress, mitochondrial dysfunction, serotonin transporter (5-HTT), serotonin receptor 7 (5-HTR7), tumor necrosis factor α (TNF), and interleukin 6 (IL-6) levels. Immunohistochemical staining for glial fibrillary acidic protein (GFAP) was also performed to assess astrocytic reaction. Results: KV-treated VPA-exposed rats showed significant improvements in social interaction and with lower repetitive behavior. Biochemically, KV decreased malondialdehyde (MDA), IL-6 and TNFα levels, improved catalase activity and mitochondrial membrane potential (MMP), and modulated serotonergic markers (5-HTT and 5-HTR7). Histologically, KV also attenuated hippocampal GFAP immunoreactivity (IRA). Conclusion: KV showed its promising potential as a complementary therapeutic agent in ASD murine model. Further studies are still warranted to clarify its further mechanisms and clinical relevance.
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