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纳米硒通过降低氧化应激和激活雄性昆明小鼠的Nrf2信号通路减轻镉诱导的急性肝毒性

Nano-Selenium Alleviates Cadmium-Induced Acute Hepatic Toxicity by Decreasing Oxidative Stress and Activating the Nrf2 Pathway in Male Kunming Mice.

作者信息

Du Hong, Zheng Yilei, Zhang Wei, Tang Huaqiao, Jing Bo, Li Haohuan, Xu Funeng, Lin Juchun, Fu Hualin, Chang Lijen, Shu Gang

机构信息

Department of Basic Veterinary Medicine, Sichuan Agricultural University, Chengdu, China.

College of Veterinary Medicine, University of Minnesota, St Paul, MN, United States.

出版信息

Front Vet Sci. 2022 Jul 26;9:942189. doi: 10.3389/fvets.2022.942189. eCollection 2022.

Abstract

Cadmium (Cd) is known as a highly toxic heavy metal and has been reported to induce hepatotoxicity in animals. Nano-selenium (NSe) is an antioxidant that plays many biological roles such as oxidative stress alleviation. The purpose of this study is to explore the mechanism of action by which NSe inhibits Cd-induced hepatic toxicity and oxidative stress. Sixty eight-week-old male Kunming mice were randomly divided into four groups (15 mice per group). The control group and cadmium groups received distilled water, whereas the sodium-selenite group received 0.2 mg/kg SSe and the NSe group received 0.2 mg/kg NSe intragastrically for 2 weeks. On the last day, all the other groups were treated with Cd (126 mg/kg) except for the control group. The results obtained in this study showed that NSe alleviated Cd-induced hepatic pathological changes. Furthermore, NSe reduced the activities of ALT and AST as well as the content of MDA, while elevated the activities of T-AOC, T-SOD and GSH ( < 0.05). In addition, the NSe group significantly increased mRNA expressions of Nrf2 pathway related molecules (Nrf2, HO-1, NQO-1, GST, GSH-Px, CAT and SOD) compared to the Cd group ( < 0.05). In conclusion, NSe shows its potentiality to reduce Cd-induced liver injury by inhibiting oxidative stress and activating the Nrf2 pathway.

摘要

镉(Cd)是一种剧毒重金属,据报道可在动物体内诱发肝毒性。纳米硒(NSe)是一种抗氧化剂,具有许多生物学作用,如减轻氧化应激。本研究的目的是探讨NSe抑制Cd诱导的肝毒性和氧化应激的作用机制。将68只8周龄雄性昆明小鼠随机分为四组(每组15只)。对照组和镉组给予蒸馏水,而亚硒酸钠组给予0.2mg/kg亚硒酸钠,NSe组给予0.2mg/kg NSe灌胃2周。在最后一天,除对照组外,所有其他组均用Cd(126mg/kg)处理。本研究结果表明,NSe减轻了Cd诱导的肝脏病理变化。此外,NSe降低了ALT和AST的活性以及MDA的含量,同时提高了T-AOC、T-SOD和GSH的活性(P<0.05)。此外,与Cd组相比,NSe组显著增加了Nrf2通路相关分子(Nrf2、HO-1、NQO-1、GST、GSH-Px、CAT和SOD)的mRNA表达(P<0.05)。总之,NSe通过抑制氧化应激和激活Nrf2通路显示出减轻Cd诱导的肝损伤的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ac1e/9362431/1591aa8f26fa/fvets-09-942189-g0001.jpg

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