抗氧化剂通过激活Nrf2-keap1及其相关通路减轻铬镉联合诱导的瑞士白化病小鼠神经毒性和细胞凋亡的作用。

IF 3.2 3区 医学 Q2 ENDOCRINOLOGY & METABOLISM
Swapnil Tripathi, Dharati Parmar, Samir Raval, Shivkumar Prajapati, Gyanendra Singh
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引用次数: 0

摘要

铬(Cr)和镉(Cd)是众所周知的在生物圈中共存的细胞毒性和致癌元素。虽然它们各自的毒性已经得到了很好的研究,但对它们的综合作用,特别是对细胞应激反应的影响知之甚少。本研究旨在探索铬和镉在瑞士白化小鼠大脑中的单独和联合毒性作用,以及检测辅酶Q10 (CoQ10)、生物茶素a (BCA)和根皮素(PHL)可能的神经保护功能,这些天然存在的具有抗氧化特性的类黄酮。小鼠口服Cr和Cd(各75 ppm),同时口服辅酶q10(各10 mg/kg)、BCA和PHL(各50 mg/kg)。治疗两周后,进行了一系列生化分析、组织病理学检查和基因表达分析,以评估所选营养保健品的潜在机制。我们的研究结果强调了本研究的重要性,表明营养保健品的管理通过降低丙二醛(MDA)和蛋白质羰基含量(PCC)的水平,同时增加超氧化物歧化酶(SOD),过氧化氢酶(CAT),谷胱甘肽- s转移酶(GST),还原型谷胱甘肽(GSH)和总硫醇(TT)活性来降低氧化应激并恢复抗氧化防御系统。胆碱酯酶活性降低,组织结构改变。mRNA表达的qRT-PCR分析显示,抗氧化防御相关基因SIRT1、Nrf2、HO-1、NQO1表达上调,凋亡标志物caspase-8和3表达下调。该研究强调了CoQ10、BCA和PHL通过增强nrf2介导的外源性抗氧化防御和减轻细胞损伤和神经凋亡,对Cr和cd诱导的氧化应激具有神经保护作用。这些结果表明,这些营养保健品可能在减轻重金属暴露引起的神经系统疾病方面具有治疗价值,并对未来的治疗产生潜在的重大影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Alleviating effect of antioxidants on combined chromium and cadmium-induced neurotoxicity and apoptosis by activating the Nrf2-keap1 and associated pathway in Swiss albino mice.

Chromium (Cr) and cadmium (Cd) are well-known cytotoxic and carcinogenic elements co-existing in the biosphere. Though their separate toxicities have been well researched, little is known about their combined effects, particularly with regard to the cellular stress response. The current study intends to explore the individual and combined toxic effects of Cr and Cd in the brain of Swiss albino mice in addition to examining the possible neuroprotective functions of coenzyme Q10 (CoQ10), biochanin-A (BCA), and phloretin (PHL), the naturally occurring flavonoids with antioxidant qualities. Mice were administered orally with Cr and Cd (75 ppm each) along with the i.p. dose of CoQ10 (10 mg/kg), BCA, and PHL (50 mg/kg each), respectively. After two weeks of treatment, an array of biochemical assays, histopathological examination, and gene expression analyses were carried out to evaluate the underlying mechanisms of the selected nutraceuticals. Our findings, which underscore the importance of this research, demonstrated that the administration of the nutraceuticals reduced oxidative stress and restored the antioxidant defense system by decreasing the levels of malondialdehyde (MDA) and protein carbonyl content (PCC) with concomitant increase in superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), reduced glutathione (GSH), and total thiol (TT) activity. A decrease in cholinesterase activity was also observed, along with the altered histo-architecture. The qRT-PCR analysis of mRNA expression revealed the upregulation of genes associated with antioxidant defense (SIRT1, Nrf2, HO-1, NQO1) along with the downregulation of the apoptotic markers caspase-8 and 3, respectively. The study highlights the neuroprotective effects of CoQ10, BCA, and PHL against Cr and Cd-induced oxidative stress via enhancing Nrf2-mediated exogenous antioxidant defenses and mitigating cellular damage and neural apoptosis. These results imply that these nutraceuticals may have therapeutic value in alleviating neurological disorders brought on by heavy metal exposure, with potential significant impact on future treatments.

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来源期刊
Metabolic brain disease
Metabolic brain disease 医学-内分泌学与代谢
CiteScore
5.90
自引率
5.60%
发文量
248
审稿时长
6-12 weeks
期刊介绍: Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experimental and clinical techniques and methodologies. Metabolic Brain Disease is directed to physicians, neuroscientists, internists, psychiatrists, neurologists, pathologists, and others involved in the research and treatment of a broad range of metabolic brain disorders.
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