Amphora coffeaeformis supplementation attenuates cypermethrin-triggered neurotoxicity, oxidative deficit, proinflammatory and apoptotic‑associated genes dysregulation, and histopathology in the brain of nile tilapias.

Cypermethrin (CYP), a neurotoxic pesticide, is released into the environment uncontrollably, posing a particular threat to aquatic species. Amphora coffeaeformis was demonstrated to have a protective effect against hazardous CYP exposure by markedly reducing neurotoxicity in Oreochromis niloticus. A total of 240 O. niloticus were divided equally into four groups in triplicate as follows: Control, AMP (5% A. coffeaeformis/kg diet), CYP (1.25 µg/L), and AMP + CYP (5% A. coffeaeformis/kg diet + 1.25 µg/L). Our data showed that CYP exposure for 30 days induced a significant decrease in γ-aminobutyric acid, acetylcholinesterase, reduced glutathione, superoxide dismutase, and catalase activities, and total antioxidant capacity in brain tissue, as well as in serum levels of lysozyme, total immunoglobulin, and nitric oxide. There was also a notable increase in brain malondialdehyde and serum cortisol and glucose levels. The qPCR analysis demonstrated a significant up-regulation of IL1β, TNFα, HSP70, and Cas3 mRNA expression in brain tissue. Importantly, A. coffeaeformis significantly shielded against CYP-induced brain impairments, including neuronal degeneration, spongiosis, perivascular edema, and inflammation. These alterations were markedly reduced following dietary exposure to A. coffeaeformis, as confirmed by IHC data. Our data examined the neuroprotective effects of A. coffeaeformis in CYP-exposed fish, supporting its potential as an anti-inflammatory, antioxidant, and neuroprotective agent.