为探究酵母硒（Se-Y）对黄曲霉毒素B1（AFB1）诱导的鹌鹑肝脏损伤的缓解作用，将20日龄的雌性黄羽鹌鹑按每组10只，随机分为对照组（基础日粮）、Se-Y组（0.8 mg/kg Se-Y）、AFB1组（30 μg/kg B.W AFB1）和Se-Y+AFB1组（0.8 mg/kg Se-Y+30 μg/kg B.W AFB1），检测其肝脏组织病理损伤情况，血清生化、肝脏组织氧化与抗氧化指标，肝脏组织Nrf2信号通路相关基因表达情况。结果显示，与对照相比，AFB1暴露会导致鹌鹑肝脏出现肿大、发黄、发白和易碎的现象，病理学观察表现为细胞索排列混乱，肝细胞肿胀和空泡化变性等病理变化；血清中谷草转氨酶（AST）和谷丙转氨酶（ALT）活性明显增加，肝脏组织中的丙二醛（MDA）和过氧化氢（H₂O₂）的含量均明显升高，谷胱甘肽过氧化物酶（GSH-Px）、总超氧化物歧化酶（T-SOD）和过氧化氢酶（CAT）活性均明显降低，总抗氧化能力（T-AOC）水平降低；Nrf2信号通路相关基因（Nrf2，HO-1，NQO-1，SOD1，CAT）的表达受到明显抑制。与AFB1组相比，Se-Y+AFB1组减轻了AFB1导致的肝脏组织病理损伤，血清中的AST和ALT活性有所降低，肝脏组织中GSH-Px、CAT和T-SOD活性及T-AOC水平有所升高；而Nrf2信号通路相关基因的表达量有所增加。综上所述，AFB1暴露诱导鹌鹑肝脏氧化应激，抑制Nrf2信号通路相关基因的表达，导致肝脏损伤，而Se-Y通过增强Nrf2相关基因的表达来拮抗AFB1所诱导的鹌鹑肝脏氧化损伤，但具体机制仍需进一步研究。

To investigate the potential mitigating effects of yeast selenium (Se-Y) on aflatoxin B1 (AFB1)-induced liver injury in quails, 20-day-old female yellow-feathered quails were randomly divided into four groups (10 quails per group): control group (basic daily ration), Se-Y group (0.8 mg/kg Se-Y), AFB1 group (30 μg/kg B.W AFB1), and Se-Y+AFB1 antagonism group (0.8 mg/kg Se-Y+30 μg/kg B.W AFB1). Liver histopathological damage, serum biochemical parameters, hepatic oxidative and antioxidant indices, and the expression levels of genes related to the Nrf2 signaling pathway were assessed.The results showed that compared with the control group, AFB1 exposure caused the quail livers to exhibit swelling, yellowing, whitening, and fragility. Histopathological observations revealed disordered cell cord arrangements, hepatocyte swelling, and vacuolar degeneration. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities were significantly increased. In liver tissues, malondialdehyde (MDA) and hydrogen peroxide (H₂O₂) levels were markedly elevated, while glutathione peroxidase (GSH-Px), total superoxide dismutase (T-SOD), and catalase (CAT) activities were significantly reduced. Additionally, total antioxidant capacity (T-AOC) was decreased. The expression of Nrf2 signaling pathway related genes (Nrf2, HO-1, NQO-1, SOD1, CAT) was significantly suppressed. Compared with the AFB1 group, the Se-Y+AFB1 antagonism group alleviated AFB1-induced liver histopathological damage, reduced serum AST and ALT activities, and increased hepatic GSH-Px, CAT, and T-SOD activities as well as T-AOC levels. Furthermore, the expression of Nrf2 signaling pathway related genes were upregulated.In conclusion, AFB1 exposure induces oxidative stress in quail livers and suppresses the expression of Nrf2 signaling pathway-related factors, leading to liver injury. Se-Y counteracts AFB1-induced hepatic oxidative damage by enhancing the expression of Nrf2-related factors, though the precise mechanisms require further investigation.