Chemico-biological interactions · 2026
Integrated pathways of T-2 toxin-induced neurotoxicity and protection by sodium butyrate in quails.
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Cao Changyu, Huang Chuying, Li Xinran
Аннотация
BACKGROUND: T-2 toxin, a prevalent mycotoxin in feed, poses severe health risks to poultry. While its systemic toxicity is recognized, its neurotoxic effects in birds, and effective countermeasures, remain underexplored. Sodium butyrate (NaB), a green feed additive, has shown broad biological benefits, but its potential to alleviate T-2-induced neurotoxicity is unclear.
OBJECTIVE: This study aimed to investigate the neurotoxic mechanisms of T-2 toxin in quails and evaluate the protective role of sodium butyrate.
METHODS: Two-hundred-and-forty 10-day-old quails were randomly assigned to Control, T-2 toxin (0.9 mg/kg), NaB (500 mg/kg), and T-2+NaB groups. After 14 and 28 days, brain tissues were collected for histopathological (hematoxylin-eosin [HE], Nissl, Fluoro-Jade B [FJB] staining) and molecular analyses (RT-qPCR, Western blot, semi-quantitative PCR) to assess oxidative stress, inflammation, and endoplasmic reticulum (ER) stress.
RESULTS: T-2 toxin induced severe brain damage, characterized by neuronal vacuolization, loss of Nissl bodies, and degeneration. It concurrently activated oxidative stress (upregulated Nrf2 [nuclear factor erythroid 2-related factor 2], HO-1 [heme oxygenase-1], NQO1 [NAD(P)H: quinone oxidoreductase 1]), neuroinflammation (elevated TNF-α [tumor necrosis factor-alpha], IL-1β [interleukin-1 beta], IL-6 [interleukin-6], IL-18 [interleukin-18]), and ER stress (increased GRP78 [glucose-regulated protein 78], IRE1α [inositol-requiring enzyme 1 alpha], TRAF2 [TNF receptor-associated factor 2], IKKα/β [IκB kinase alpha/beta], XBP1 [X-box binding protein 1]). Sodium butyrate supplementation significantly mitigated these histopathological alterations and downregulated the overactivated molecular pathways across all three axes.
CONCLUSION: This study demonstrates that sodium butyrate confers comprehensive neuroprotection against T-2 toxin in quails by co-ordinately alleviating oxidative stress, neuroinflammation, and ER stress. These findings provide a mechanistic basis for using NaB as a dietary intervention to combat mycotoxin-related neurotoxicity in poultry.
OBJECTIVE: This study aimed to investigate the neurotoxic mechanisms of T-2 toxin in quails and evaluate the protective role of sodium butyrate.
METHODS: Two-hundred-and-forty 10-day-old quails were randomly assigned to Control, T-2 toxin (0.9 mg/kg), NaB (500 mg/kg), and T-2+NaB groups. After 14 and 28 days, brain tissues were collected for histopathological (hematoxylin-eosin [HE], Nissl, Fluoro-Jade B [FJB] staining) and molecular analyses (RT-qPCR, Western blot, semi-quantitative PCR) to assess oxidative stress, inflammation, and endoplasmic reticulum (ER) stress.
RESULTS: T-2 toxin induced severe brain damage, characterized by neuronal vacuolization, loss of Nissl bodies, and degeneration. It concurrently activated oxidative stress (upregulated Nrf2 [nuclear factor erythroid 2-related factor 2], HO-1 [heme oxygenase-1], NQO1 [NAD(P)H: quinone oxidoreductase 1]), neuroinflammation (elevated TNF-α [tumor necrosis factor-alpha], IL-1β [interleukin-1 beta], IL-6 [interleukin-6], IL-18 [interleukin-18]), and ER stress (increased GRP78 [glucose-regulated protein 78], IRE1α [inositol-requiring enzyme 1 alpha], TRAF2 [TNF receptor-associated factor 2], IKKα/β [IκB kinase alpha/beta], XBP1 [X-box binding protein 1]). Sodium butyrate supplementation significantly mitigated these histopathological alterations and downregulated the overactivated molecular pathways across all three axes.
CONCLUSION: This study demonstrates that sodium butyrate confers comprehensive neuroprotection against T-2 toxin in quails by co-ordinately alleviating oxidative stress, neuroinflammation, and ER stress. These findings provide a mechanistic basis for using NaB as a dietary intervention to combat mycotoxin-related neurotoxicity in poultry.