Abstract
The privileges of dietary baicalin intervention as a prophylaxis were assessed in Nile tilapia (Oreochromis nilo-ticus) pre and post-acute ammonia challenge. The experimental trial lasted for 4 weeks, the first group served as a control (fed a basal diet), while, the second group received diet supplemented with baicalin (0.8 g/kg diet). The third group was fed a basal diet and exposed to acute ammonia toxicity in the last week. Meanwhile, the fourth group fed diet supplemented with baicalin (0.8 g/kg diet), then exposed to unionized ammonia challenge (5 mg/ L) in the last week. Dietary baicalin notably augmented immune indicators (lysozyme, respiratory burst activity, phagocytic activity assay, and immunoglobulin (Ig) and tissue antioxidant biomarkers (total antioxidant capacity (TAC), glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT)). Meanwhile, it decreased malon-dialdehyde (MDA), hepato-renal indicators (aspartate aminotransferase (AST), alanine aminotransferase (ALT), urea, uric acid, creatinine), and stress indicators including glucose, cholesterol, triglycerides, and cortisol. Ammonia exposure significantly elevated stress parameters and MDA, but lessened SOD, GSH, CAT, and TAC levels in liver, gills, and kidneys tissue. Dietary baicalin and ammonia exposure induced interaction impacts on urea, creatinine, cortisol, glucose, lysozyme, alanine aminotransferase (ALT), aspartate aminotransferase (AST). Prior to ammonia exposure, baicalin administration clearly decreased urea. Fish fed enriched diet with -baicalin showed no changes in stress biomarkers before ammonia exposure, meanwhile reduced it after the ammonia challenge. Dietary baicalin alleviated fluctuations induced by ammonia in all above-mentioned parameters. And alleviated the altered gene expression for Hsp70, Nf-Kappa B, Myd88, traf6, Nrf2, Ho-1, Il-1 beta, Il-8, TNF-alpha, and TLR-4 induced by ammonia toxicity. Taken together, it has been recommended to use baicalin for 3 weeks to mitigate ammonia-induced-oxidative damage, immune impairment, stress condition, hepato-renal failure, antioxidant and inflammatory gene expression in O. niloticus.