Chen Xiaoguang, Wei Wenjuan, Li Haonan, Xu Wenjing, Lv Qiongxia, Liu Yumei, Zhang Ziqiang
College of Animal Science and Technology, Henan University of Science and Technology, Luoyang 471000, China.
Toxins (Basel). 2025 May 30;17(6):275. doi: 10.3390/toxins17060275.
Zearalenone (ZEA), a mycotoxin primarily generated by the Fusarium species, constitutes a prevalent contaminant in both human and animal feedstuffs. Chronic exposure to this mycotoxin induces hepatic inflammatory responses in livestock species including rabbits, ultimately leading to organ damage. Selenomethionine (SeMet), an organic selenium source recognized for its antioxidant properties and anti-inflammatory bioactivity, demonstrates protective benefits in animals through its detoxification mechanism and growth promotion. The present study investigated the protective effect of SeMet against ZEA-induced hepatic inflammation and elucidated its underlying mechanisms. Fifty healthy 90-day-old rabbits were randomly divided into five groups: control, ZEA-exposed and three SeMet-supplemented groups receiving 0.2, 0.35 or 0.5 mg/kg via dietary inclusion. After two weeks of SeMet pretreatment, ZEA administration (1.2 mg/kg B.W.) was imitated via oral gavage daily for one week in both the ZEA group and three SeMet-treated groups. As a result, ZEA exposure induced the significant structural disruption of the hepatic lobules, accompanied by increased collagen deposition, elevated pro-inflammatory cytokine profiles (IL-6, IL-1β, TNF-α) and reduced anti-inflammatory mediator levels (IL-10, TGF-β). SeMet supplementation alleviated ZEA-induced histological alterations, including inflammatory cell infiltration and collagen accumulation. Biochemical analysis indicated the restoration of inflammatory markers to near-normal levels when treated with SeMet. Notably, immunohistochemical results showed that SeMet significantly reduced the protein levels of IL-6 and its downstream target STAT3 under ZEA exposure. These findings indicated that SeMet attenuated ZEA-induced hepatic inflammation by modulating the IL-6/STAT3 signaling axis, with dietary supplementation of 0.35 mg/kg SeMet exhibiting the most significant effect on alleviating ZEA-induced hepatic inflammatory injury.
玉米赤霉烯酮（ZEA）是一种主要由镰刀菌属产生的霉菌毒素，是人和动物饲料中普遍存在的污染物。长期接触这种霉菌毒素会在包括兔子在内的家畜物种中引发肝脏炎症反应，最终导致器官损伤。硒代蛋氨酸（SeMet）是一种有机硒源，以其抗氧化特性和抗炎生物活性而闻名，通过其解毒机制和促进生长作用对动物具有保护作用。本研究调查了SeMet对ZEA诱导的肝脏炎症的保护作用，并阐明了其潜在机制。将50只健康的90日龄兔子随机分为五组：对照组、ZEA暴露组和三个通过日粮添加分别接受0.2、0.35或0.5 mg/kg SeMet的补充组。在SeMet预处理两周后，ZEA组和三个SeMet处理组每天通过口服灌胃模拟给予ZEA（1.2 mg/kg体重），持续一周。结果，ZEA暴露导致肝小叶结构明显破坏，伴有胶原蛋白沉积增加、促炎细胞因子水平（IL-6、IL-1β、TNF-α）升高和抗炎介质水平降低（IL-10、TGF-β）。补充SeMet减轻了ZEA诱导的组织学改变，包括炎症细胞浸润和胶原蛋白积累。生化分析表明，用SeMet治疗后炎症标志物恢复到接近正常水平。值得注意的是，免疫组化结果显示，在ZEA暴露下，SeMet显著降低了IL-6及其下游靶点STAT3的蛋白水平。这些发现表明，SeMet通过调节IL-6/STAT3信号轴减轻了ZEA诱导的肝脏炎症，日粮补充0.35 mg/kg SeMet对减轻ZEA诱导的肝脏炎症损伤效果最为显著。
