Crosslinking Apigenin with Neurodevelopment: In-Vivo Model Designing based Therapeutic Strategy for Autism-Associated Neuroinflammation

Background: Autism Spectrum Disorder (ASD) is a complex neurodevelopmental disorder characterized by impaired social interaction, communication difficulties, and repetitive behaviors. Neuroinflammation is increasingly recognized as a key contributor to ASD pathophysiology. Nerve Growth Factor (NGF), a vital neurotrophin involved in neuronal survival and plasticity, is often dysregulated in ASD, exacerbating neurological dysfunction. Apigenin, a natural flavonoid with known anti-inflammatory and neuroprotective properties, has shown promise as a therapeutic agent in neurodevelopmental conditions. This study evaluated the effects of apigenin treatment on autism-like neuroinflammation by examining its impact on NGF regulation in a rodent model. Methods: This in vivo study (July–November 2021) used 20 healthy male rats (8 weeks old). The research took place within the Animal House facility and was analyzed at SMDC Lahore and LUMHS Jamshoro, Sindh. Group I (n=4) was taken as control, while Groups II–V (n=16) received 250 mg/kg/day propionic acid (PPA) to induce autism-like neuroinflammation. Groups III–V were treated with Apigenin at 50, 100, and 200 mg/kg. NGF serum levels were analyzed using the enzyme-linked immunosorbent assay (ELISA). SPSS v 21 was used for statistical analysis using one-way ANOVA and Tukey’s test. p<0.05 was taken as significant. Results: The levels of NGF were significantly lowered using propanoic acid (PPA) (4.3 ± 0.5 pg/mL vs control 11.9 ± 0.5). Apigenin dose-dependently restored NGF, with Group V (200 mg/kg) reaching 9.8 ± 0.5 pg/mL. Conclusion: The neuroprotective properties of apigenin are evident through its ability to restore PPA-damaged levels of NGF, thus establishing potential use as an autism treatment for neuroinflammation in neurodevelopmental disorders.