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Protection Mechanisms Underlying Oral Administration of Chlorogenic Acid against Cadmium-Induced Hepatorenal Injury Related to Regulating Intestinal Flora Balance

机译:口服对镉诱导的Hepatorenal损伤口服施用的保护机制与调节肠道菌群平衡相关

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摘要

Cadmium (Cd) is a heavy metal, which is widely used in the industry and daily life. It has a long half-life, so large amounts of Cd can accumulate in humans and become toxic. Chlorogenic acid (CGA) can eliminate free radicals and inhibit lipid peroxidation and is mainly used to prevent metal toxicity. In the present study, mice are given CGA by intraperitoneal injection or gavage, respectively, to explore the mechanism of preventing Cd toxicity. In acute Cd-exposed mice, CGA treatment (ip) alleviated Cd-induced oxidative damage and reduced the production of NO and MPO in the liver and kidney tissues, while TLR4 expression levels did not change significantly. After 8 weeks of Cd exposure, CGA administration (gavage) significantly alleviated gut dysbiosis by decreasing the Firmicutes to Bacteroidetes ratio, enhancing the relative abundances of bacteria, including Ruminiclostridium_9 , Alloprevotella , and Rikenella , and inhibiting the activation of the TLR4/MyD88/NF-κB signaling pathway. These findings suggested that protection mechanisms underlying the oral administration of CGA against the Cd-induced hepatorenal injury was related to the regulation of the intestinal flora balance. CGA can be used as an effective component in daily diet to prevent Cd toxicity.
机译:镉(Cd)是一种重金属,广泛应用于工业和日常生活中。它有很长的半衰期,因此大量的镉会在人体内积累并产生毒性。绿原酸(CGA)能清除自由基,抑制脂质过氧化,主要用于防止金属毒性。在本研究中,小鼠分别通过腹腔注射或灌胃给予CGA,以探索预防Cd毒性的机制。在急性镉暴露小鼠中,CGA治疗(ip)减轻了镉诱导的氧化损伤,减少了肝和肾组织中NO和MPO的产生,而TLR4的表达水平没有显著变化。在镉暴露8周后,CGA给药(灌胃)通过降低厚壁菌与类杆菌的比率,增加细菌的相对丰度,包括反刍梭菌9、异丙雷维菌和里肯内拉,并抑制TLR4/MyD88/NF-κB信号通路的激活,显著缓解肠道失调。这些发现表明,口服CGA对镉诱导的肝肾损伤的保护机制与调节肠道菌群平衡有关。CGA可以作为日常饮食中的有效成分来防止镉中毒。

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