Hesperidin Attenuates Acrylamide‐Induced Ovarian Toxicity in Rats: Based on Network Pharmacology, Molecular Docking, and In Vivo Studies

Exposure to acrylamide (AA) through food is nearly unavoidable and can lead to long-lasting consequences. AA has been shown to cause reproductive toxicity and reduce ovarian weight and follicle number when taken orally. Flavonoids derived from plants are bioactive compounds that are increasingly being used in medicine. In this research, we aimed to investigate the ability of hesperidin (HES), a bioactive compound derived from plants, in shielding rats from AA-induced ovarian damage. We identified possible target genes related to HES therapy and AA toxicity and conducted functional enrichment and pathway analysis to understand their biological significance. Additionally, we performed molecular docking of the core target gene with AA and HES. During the animal experimentation, rats were first exposed to 40 mg/kg of AA orally for 10 days and then received HES therapy at various doses for three consecutive days. All animals were euthanised 24 h after receiving the final treatment. We evaluated reproductive hormones, oxidative stress markers, membrane-bound enzymes, glycogen content, and histological findings to determine the protective efficacy of HES. The study found that HES has a high binding affinity with the core target proteins and showed impressive protection against oxidative damage induced by AA in our in vivo experiment. This protection can likely be attributed to HES's potent antioxidant properties.