甘露寡糖对镉致大鼠肝脏氧化损伤的保护作用。

IF 1
E Duan, W Gao, C Liu, J Wang, J Wang, L Su, H Qiao, P Wang, J Huang, L Gan
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引用次数: 0

摘要

本研究旨在探讨甘露寡糖(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。选取雄性SD大鼠30只,随机分为5组:对照组和4组分别给予氯化镉(CdCl2) (2 mg/kg体重(b.w))和不同MOS浓度(0、100、300、500 mg/kg b.w)处理。结果表明,给药剂量为500 mg/kg的MOS可显著降低cd诱导的大鼠肝脏氧化损伤。体重增加(BWG)和胸腺指数的增加证明了这一点。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)活性显著高于单独Cd处理组。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)、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Nrf2基因表达水平升高,血红素加氧酶1 (HO-1)和醌氧化还原酶1 (NQO1) mRNA表达水平降低。综上所述,MOS可有效减轻cd诱导的大鼠肝脏氧化损伤,且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。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protective effect of mannose oligosaccharides on cadmium-induced hepatic oxidative damage in rats.

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.

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