Duan E, Gao W, Liu C, Wang J, Wang J, Su L, Qiao H, Wang P, Huang J, Gan L
College of Biological Engineering, Henan University of Technology, 100 Lianhua Street, Hi-tech Zone, Zhengzhou 450001, Henan, China.
Pol J Vet Sci. 2025 Jun;28(2):311-320. doi: 10.24425/pjvs.2025.154952.
The objective of this study was to investigate the effect of mannose oligosaccharides (MOS) against cadmium (Cd)-induced hepatic oxidative damage and analyze its underlying antioxidant mechanism. Thirty male Sprague-Dawley (SD) rats were randomly divided into five groups: control group and four others treated with cadmium chloride (CdCl2) (2 mg/kg body weight (b.w.)) and different MOS levels at 0, 100, 300, 500 mg/kg b.w.. The results demonstrated that administration of MOS at a dose of 500 mg/kg significantly reduced Cd-induced oxidative damage in rat livers. This was evidenced by an increase in body weight gain (BWG) and thymus index. Additionally, liver superoxide dismutase (SOD), catalase (CAT) and total antioxidant capacity (T-AOC) activities were significantly improved compared to the group exposed to Cd alone. Conversely, MOS resulted in significant reductions in the liver index, liver malondialdehyde (MDA), hydrogen peroxide (H2O2), glutathione (GSH), and serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Morphological analysis showed that MOS ameliorated Cd-induced histopathology of the rat liver. Notably, Nrf2 gene expression levels increased, while heme oxygenase 1 (HO-1) and quinone oxidoreductase 1 (NQO1) mRNA levels decreased in the MOS group. In conclusion, MOS effectively attenuate Cd-induced oxidative damage in rat liver and the Nrf2 signaling pathway is involved in this process. This study provides valuable insights for the implementation of MOS applications in livestock and poultry production.
本研究的目的是探讨甘露寡糖(MOS)对镉(Cd)诱导的肝脏氧化损伤的影响,并分析其潜在的抗氧化机制。将30只雄性Sprague-Dawley(SD)大鼠随机分为五组:对照组和其他四组,分别给予氯化镉(CdCl2)(2 mg/kg体重(b.w.))和不同剂量的MOS(0、100、300、500 mg/kg b.w.)。结果表明,500 mg/kg剂量的MOS给药显著降低了Cd诱导的大鼠肝脏氧化损伤。体重增加(BWG)和胸腺指数增加证明了这一点。此外,与单独暴露于Cd的组相比,肝脏超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和总抗氧化能力(T-AOC)活性显著提高。相反,MOS导致肝脏指数、肝脏丙二醛(MDA)、过氧化氢(H2O2)、谷胱甘肽(GSH)以及血清丙氨酸转氨酶(ALT)和天冬氨酸转氨酶(AST)水平显著降低。形态学分析表明,MOS改善了Cd诱导的大鼠肝脏组织病理学。值得注意的是,MOS组中Nrf2基因表达水平升高,而血红素加氧酶1(HO-1)和醌氧化还原酶1(NQO1)mRNA水平降低。总之,MOS有效减轻了Cd诱导的大鼠肝脏氧化损伤,Nrf2信号通路参与了这一过程。本研究为MOS在畜禽生产中的应用提供了有价值的见解。