Zhou Jing, Lv Wenting, Li Zhonghao, Wang Li, Guo Bing, Du Donghua
Department of Veterinary Medicine, College of Animal Science and Technology, Hebei North University, Zhangjiakou 075131, China.
Foods. 2025 Aug 8;14(16):2758. doi: 10.3390/foods14162758.
Heat stress (HS) is known to cause liver injury through mechanisms involving oxidative stress and inflammation, thereby highlighting the need for effective therapeutic interventions. This study evaluated the efficacy of sprouted black quinoa extract (SBQE) in mitigating HS-induced liver injury in a rat model. SBQE was obtained through an ultrasonication-assisted ethanol-water extraction process from black quinoa germinated for 48 h. Sprague Dawley rats (male) were administered via oral gavage SBQE at doses of 200, 400, or 800 mg/kg prior to each HS exposure (40 °C for 2 h per day over a period of 8 days). Pretreatment with SBQE resulted in a dose-dependent reduction in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, with the high dose (800 mg/kg) reducing these enzyme levels ( < 0.001 vs. HS group) and alleviating histopathological damage, including a significant decrease in hepatocyte vacuolization and inflammatory cell infiltration (histopathological scores were reduced by < 0.001 in the 800 mg/kg SBQE group vs. HS group). SBQE also dose-dependently inhibited the accumulation of mitochondrial reactive oxygen species (mean fluorescence intensity decreased by < 0.001 at 800 mg/kg) and the formation of malondialdehyde while restoring the activities of antioxidant enzymes such as superoxide dismutase ( < 0.01 at 800 mg/kg), catalase ( < 0.05 at 800 mg/kg), and glutathione peroxidase ( < 0.001 at 800 mg/kg), as well as replenishing glutathione levels ( < 0.001 at 800 mg/kg). Furthermore, the levels of proinflammatory cytokines (tumor necrosis factor-alpha, interleukin-6, interleukin-1β, and interleukin-18) in liver tissue were significantly reduced (with the high dose leading to < 0.001 vs. HS group), which was associated with enhanced nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2; < 0.05 at 800 mg/kg) and decreased phosphorylation of nuclear factor-κB p65 (NF-κB; < 0.001 at 800 mg/kg). Additionally, the protein expression of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome components and markers of apoptosis were diminished. The results demonstrated that SBQE alleviated HS-induced liver injury by concurrently activating the Nrf2 antioxidant pathway and suppressing NF-κB/NLRP3 inflammasome signaling, suggesting its potential as a nutraceutical intervention for HS-related hepatotoxicity.
已知热应激（HS）通过涉及氧化应激和炎症的机制导致肝损伤，因此凸显了有效治疗干预措施的必要性。本研究评估了发芽黑藜麦提取物（SBQE）在减轻大鼠模型中HS诱导的肝损伤方面的功效。SBQE是通过超声辅助乙醇-水提取工艺从发芽48小时的黑藜麦中获得的。在每次HS暴露（40℃，每天2小时，持续8天）之前，通过灌胃法给雄性Sprague Dawley大鼠施用200、400或800mg/kg剂量的SBQE。SBQE预处理导致血清丙氨酸氨基转移酶（ALT）和天冬氨酸氨基转移酶（AST）水平呈剂量依赖性降低，高剂量（800mg/kg）降低了这些酶的水平（与HS组相比，P<0.001），并减轻了组织病理学损伤，包括肝细胞空泡化和炎性细胞浸润显著减少（800mg/kg SBQE组与HS组相比，组织病理学评分降低了P<0.001）。SBQE还呈剂量依赖性地抑制线粒体活性氧的积累（800mg/kg时平均荧光强度降低了P<0.001）和丙二醛的形成，同时恢复了超氧化物歧化酶（800mg/kg时P<0.01）、过氧化氢酶（800mg/kg时P<0.05）和谷胱甘肽过氧化物酶（800mg/kg时P<0.001）等抗氧化酶的活性，并补充了谷胱甘肽水平（800mg/kg时P<0.001）。此外，肝组织中促炎细胞因子（肿瘤坏死因子-α、白细胞介素-6、白细胞介素-1β和白细胞介素-18）的水平显著降低（高剂量导致与HS组相比P<0.001），这与核因子红细胞2相关因子2（Nrf2）的核转位增强（800mg/kg时P<0.05）和核因子-κB p65（NF-κB）的磷酸化降低（800mg/kg时P<0.001）有关。此外，含NOD样受体吡咯结构域3（NLRP3）炎性小体成分的蛋白表达和凋亡标志物减少。结果表明，SBQE通过同时激活Nrf2抗氧化途径和抑制NF-κB/NLRP3炎性小体信号传导减轻了HS诱导的肝损伤，表明其作为HS相关肝毒性的营养干预措施具有潜力。
