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Involvement of Nrf2 and mitochondrial apoptotic signaling in trehalose protection against cadmium-induced kidney injury
Metallomics ( IF 2.9 ) Pub Date : 2020-11-3 , DOI: 10.1039/d0mt00213e Rui-Feng Fan 1 , Zi-Fa Li , Dong Zhang , Zhen-Yong Wang
Metallomics ( IF 2.9 ) Pub Date : 2020-11-3 , DOI: 10.1039/d0mt00213e Rui-Feng Fan 1 , Zi-Fa Li , Dong Zhang , Zhen-Yong Wang
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Cadmium (Cd) poisoning is characterized by multiple organ dysfunction in organisms, and the kidney is the main target organ of Cd toxicity. Trehalose (Tr), a multifunctional bioactive disaccharide, possesses potential kidney protective properties. Nevertheless, the specific biological function of Tr in antagonizing kidney injury induced by Cd remains to be elucidated. Herein, an in vivo model of Tr antagonizing Cd nephrotoxicity was established and the indictors related to kidney function, oxidative stress, and apoptosis were detected to investigate the molecular mechanism underlying the Tr-protection against Cd-induced kidney injury of rats. Firstly, Tr significantly declined the levels of blood urea nitrogen (BUN) and serum creatinine, and partially restored renal pathological changes caused by Cd. Secondly, Cd exposure significantly increased the malondialdehyde (MDA) content, and decreased the levels of total antioxidant capacity (T-AOC), superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT), and glutathione (GSH) in serum. However, Tr significantly ameliorated these abnormal alterations. Moreover, Tr regulated the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway to suppress the Cd-induced nuclear translocation of Nrf2 and the up-regulation of heme oxygenase-1 (HO-1) and NAD (P) H quinone reductase-1 (NQO1). Meanwhile, Tr significantly reversed the increased Sequestosome-1(SQSTM1/p62) and decreased Kelch-like ECH associated protein-1 (Keap1) protein levels induced by Cd. Thirdly, further mechanistic exploration suggested that Tr inhibited the mitochondrial apoptotic signaling pathway induced by Cd. Collectively, the results indicated that Tr exerts antioxidant and anti-apoptosis functions involving the Nrf2 and mitochondrial apoptotic signaling pathways to protect against Cd-induced kidney injury in rats.
中文翻译：
Nrf2 和线粒体凋亡信号参与海藻糖对镉诱导的肾损伤的保护
镉（Cd）中毒的特点是机体多器官功能障碍，肾脏是镉中毒的主要靶器官。海藻糖 (Tr) 是一种多功能生物活性二糖，具有潜在的肾脏保护特性。然而，Tr在拮抗Cd诱导的肾损伤中的具体生物学功能仍有待阐明。在此，体内建立Tr拮抗Cd肾毒性模型，检测肾功能、氧化应激、细胞凋亡相关指标，探讨Tr对Cd致大鼠肾损伤的保护作用的分子机制。首先，Tr显着降低血尿素氮（BUN）和血清肌酐水平，部分恢复由Cd引起的肾脏病理变化。其次，镉暴露显着增加丙二醛（MDA）含量，并降低总抗氧化能力（T-AOC）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）、过氧化氢酶（CAT）和谷胱甘肽（GSH）的水平。血清。然而，Tr 显着改善了这些异常改变。而且，Tr 调节核因子红细胞 2 相关因子 2 (Nrf2) 信号通路以抑制 Cd 诱导的 Nrf2 核易位和血红素加氧酶-1 (HO-1) 和 NAD (P) H 醌还原酶的上调。 1 (NQO1)。同时，Tr 显着逆转了增加的 Sequestosome-1（SQSTM1/p62）并降低了由 Cd 诱导的 Kelch 样 ECH 相关蛋白 1（Keap1）蛋白水平。第三，进一步的机制探索表明，Tr 抑制 Cd 诱导的线粒体凋亡信号通路。总的来说，结果表明 Tr 发挥抗氧化和抗细胞凋亡功能，涉及 Nrf2 和线粒体凋亡信号通路，以防止大鼠 Cd 诱导的肾损伤。
更新日期：2021-01-06
中文翻译：
Nrf2 和线粒体凋亡信号参与海藻糖对镉诱导的肾损伤的保护
镉（Cd）中毒的特点是机体多器官功能障碍，肾脏是镉中毒的主要靶器官。海藻糖 (Tr) 是一种多功能生物活性二糖，具有潜在的肾脏保护特性。然而，Tr在拮抗Cd诱导的肾损伤中的具体生物学功能仍有待阐明。在此，体内建立Tr拮抗Cd肾毒性模型，检测肾功能、氧化应激、细胞凋亡相关指标，探讨Tr对Cd致大鼠肾损伤的保护作用的分子机制。首先，Tr显着降低血尿素氮（BUN）和血清肌酐水平，部分恢复由Cd引起的肾脏病理变化。其次，镉暴露显着增加丙二醛（MDA）含量，并降低总抗氧化能力（T-AOC）、超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GPx）、过氧化氢酶（CAT）和谷胱甘肽（GSH）的水平。血清。然而，Tr 显着改善了这些异常改变。而且，Tr 调节核因子红细胞 2 相关因子 2 (Nrf2) 信号通路以抑制 Cd 诱导的 Nrf2 核易位和血红素加氧酶-1 (HO-1) 和 NAD (P) H 醌还原酶的上调。 1 (NQO1)。同时，Tr 显着逆转了增加的 Sequestosome-1（SQSTM1/p62）并降低了由 Cd 诱导的 Kelch 样 ECH 相关蛋白 1（Keap1）蛋白水平。第三，进一步的机制探索表明，Tr 抑制 Cd 诱导的线粒体凋亡信号通路。总的来说，结果表明 Tr 发挥抗氧化和抗细胞凋亡功能，涉及 Nrf2 和线粒体凋亡信号通路，以防止大鼠 Cd 诱导的肾损伤。
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