Juglone’s apoptotic impact against eimeriosis-induced infection: a bioinformatics, <i>in-silico</i> , and <i>in vivo</i> approach

Abstract

Abstract Coccidiosis, induced by Eimeria spp., substantially affects gastrointestinal health and results in economic detriments. This research examined juglone (5-hydroxy-1,4-naphthoquinone), a phenolic chemical, as a prospective in-silico and in vivo apoptotic and anticoccidial potential against Eimeria papillata . For in vivo study, 25 male Swiss albino mice ( Mus musculus) were divided into five groups: CONTROL, juglone supplementation (JUG) at 8 mg/kg body weight, Infected with 1000 sporulated oocysts (INF), infected-treated with juglone (INF + JUG), and infected-treated with anticoccidial drug; amprolium (INF + DRUG). Following five days of therapy, oocyst reduction, oxidative stress, and apoptotic response evaluation were assessed. In-silico bioinformatics and molecular docking simulations analysis was conducted for juglone toward Mus musculus cysteine-aspartic acid protease-3 (caspase-3) target protein. The in vivo results indicated that E. papillata infection markedly enhanced oocyst shedding and boosted glutathione peroxidase (GPx) levels. Infection also increased the expression of caspase-3 protein and its gene expression. Juglone therapy enhanced oocyst elimination and reinstating GPx activity. It also reduced apoptosis via immunohistochemistry protein and gene expression of caspase-3. The in-silico study found that juglone interacts with caspase-3, affecting its structure and function through non-covalent interactions, potentially impairing its catalytic activity. In conclusion, juglone could serve as a promising alternative to traditional anticoccidial drugs, offering favorable anticoccidial, antioxidant and apoptotic effects against E. papillata -induced coccidiosis.