One of the oldest and most prevalent severe brain diseases is epilepsy. Cucumis melo is a member of the Cucurbitaceae family, which is used in traditional medicine to treat a variety of illnesses. The ultimate goal of this study was to examine the active constituents and mechanisms of CM against epilepsy using network pharmacology along with molecular docking technique. The chemicals in CM were determined by a review of the literature as well as the IMPPAT database. The resulting compounds were then analysed using the ADMET method. Subsequently, the STRING database was employed to design networks using the found common genes, and CB-Dock2 software was applied for docking. Out of 145 active components in CM, only 11 compounds shown outstanding potential biological activity during ADMET screening. Additionally, by accessing a number of public databases, we were able to identify 8093 genes for target chemicals and epilepsy, respectively. The results of the compounds-target network research showed that the 152 interconnected genes and 11 compounds that make up the key components and gene targets of CM against epilepsy are Eubricol and AKT1, the most prominent active component and hub protein, respectively. The metabolic pathway, reaction to xenobiotic stimulus, essential component of plasma membrane, enzyme binding, and tumour necrosis factor alpha pathways were shown to be of greatest importance based on pathway enrichment assessment. According to a molecular docking investigation, tirucallol, euphol, and eburicol demonstrated notable glide scores. Initially, we used network pharmacology and molecular docking to examine the molecular mechanisms and active components of CM for epilepsy. Our research offers empirical evidence that could bolster the medical advantages of CM; nonetheless, additional confirmation of active molecules in epilepsy treatment is necessary.

One of the oldest and most prevalent severe brain diseases is epilepsy. Cucumis melo is a member of the Cucurbitaceae family, which is used in traditional medicine to treat a variety of illnesses. The ultimate goal of this study was to examine the active constituents and mechanisms of CM against epilepsy using network pharmacology along with molecular docking technique. The chemicals in CM were determined by a review of the literature as well as the IMPPAT database. The resulting compounds were then analysed using the ADMET method. Subsequently, the STRING database was employed to design networks using the found common genes, and CB-Dock2 software was applied for docking. Out of 145 active components in CM, only 11 compounds shown outstanding potential biological activity during ADMET screening. Additionally, by accessing a number of public databases, we were able to identify 8093 genes for target chemicals and epilepsy, respectively. The results of the compounds-target network research showed that the 152 interconnected genes and 11 compounds that make up the key components and gene targets of CM against epilepsy are Eubricol and AKT1, the most prominent active component and hub protein, respectively. The metabolic pathway, reaction to xenobiotic stimulus, essential component of plasma membrane, enzyme binding, and tumour necrosis factor alpha pathways were shown to be of greatest importance based on pathway enrichment assessment. According to a molecular docking investigation, tirucallol, euphol, and eburicol demonstrated notable glide scores. Initially, we used network pharmacology and molecular docking to examine the molecular mechanisms and active components of CM for epilepsy. Our research offers empirical evidence that could bolster the medical advantages of CM; nonetheless, additional confirmation of active molecules in epilepsy treatment is necessary.