Allicin mitigates fumonisin B1-induced kidney toxicity in quails: Modulating fibrosis, NF-κB signaling pathway, and mitochondrial damage

Fumonisin B₁ (FB₁) is a common mycotoxin, which is a water-soluble metabolite produced through the metabolism of Fusarium verticillioides and Fusarium proliferator. Crops and feedstuffs are widely contaminated by FB₁ from the environment, posing risks to livestock and human health. Currently, there is no therapeutic approach available for FB₁ intoxication. Allicin, an organic sulfur compound extracted from garlic, exhibits anti-inflammatory, antioxidant, antibacterial, hepatoprotective, cardioprotective, and intestinal regulatory properties. However, investigations into allicin's role in alleviating FB₁-induced quail nephrotoxicity remain relatively limited. This study thus aimed to elucidate the mechanisms by which allicin exerts a protective effect against FB₁-induced kidney injury in juvenile quails. A total of 150 juvenile quails were randomly divided into five groups and treated with varying allicin concentrations (0, 50, 100, 500, and 1000 mg/kg) for 8 weeks. The blood and kidney tissues were subsequently screened using serum biochemical indices and histological staining, which suggested that 500 mg/kg of allicin was the optimal concentration that exerts protection to the quail kidneys. Another 120 juvenile quail were randomly divided into four groups (n = 30): control, allicin, FB₁, and allicin+FB₁. The pathological changes in kidney tissues induced by FB₁ and genes associated with nuclear xenobiotic receptors (NXRs), inflammation, fibrosis, and mitochondrial damage were evaluated after 8 weeks. FB₁ triggered kidney fibrosis and mitochondrial injury by activating the NF-κB signaling pathway, modulating NXR expression, and regulating corresponding CYP450 subtypes, which culminated in pathological injury to kidney tissues. Notably, allicin alleviated FB₁-induced kidney injury in quails, possibly by inhibiting the NF-κB pathway, fibrosis, and mitochondrial damage, suggesting the potential application of allicin in preventing FB₁-induced toxicity in quail.