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Monosodium glutamate (MSG) is widely used as a flavor enhancer and has been associated with oxidative and  reproductive disturbances in experimental models. This study investigated the protective effects of Momordica  charantia against MSG-induced ovarian toxicity in adult female Wistar rats using in vivo and in silico approaches.  Twenty-eight female Wistar rats were randomly assigned into four groups (n = 7): control, M. charantia (200  mg/kg), MSG (4 g/kg), and MSG + M. charantia. Following treatment, ovarian tissues and blood samples were  collected for histological, biochemical, and hormonal analyses. Ovarian superoxide dismutase (SOD), glutathione  peroxidase (GPx), and malondialdehyde (MDA), as well as serum follicle-stimulating hormone (FSH), luteinizing  hormone (LH), and progesterone, were assessed. Histological changes were evaluated using hematoxylin and  eosin staining. In silico screening of M. charantia bioactive compounds against the Keap1–Nrf2 protein–protein  interaction was also performed using molecular docking and related drug-likeness/ADMET analyses. MSG  administration was associated with reduced SOD and GPx activities, increased MDA levels, altered serum  reproductive hormone levels, and marked ovarian histological alterations. Treatment with M. charantia attenuated  these changes, with increased SOD and GPx, reduced MDA, improved FSH and LH levels, reduced progesterone,  and preservation of ovarian cytoarchitecture. Molecular docking identified rutin, gallic acid, caffeic acid, and  hesperidin among the top-performing compounds, with favorable predicted interactions with the Keap1–Nrf2  target. These findings suggest that M. charantia attenuates MSG-associated ovarian oxidative, hormonal, and  structural alterations, while its constituent compounds show potential interactions with the Keap1–Nrf2 pathway  that warrant further experimental investigation. 

Key Words: Monosodium glutamate, ovarian toxicity, Momordica charantia, in silico, in vivo