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抗氧化剂通过激活瑞士白化小鼠的Nrf2-keap1及相关途径对铬和镉联合诱导的神经毒性和细胞凋亡的缓解作用

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.

作者信息

Tripathi Swapnil, Parmar Dharati, Raval Samir, Prajapati Shivkumar, Singh Gyanendra

机构信息

Toxicology Department, ICMR-National Institute of Occupational Health, Ahmedabad, 380016, India.

Department of Biochemistry & Forensic Science, Gujarat University, Ahmedabad, 380009, India.

出版信息

Metab Brain Dis. 2025 Apr 4;40(4):171. doi: 10.1007/s11011-025-01594-x.

Abstract

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.

摘要

铬(Cr)和镉(Cd)是生物圈中常见的具有细胞毒性和致癌性的元素。尽管它们各自的毒性已得到充分研究,但对于它们的联合作用,尤其是在细胞应激反应方面,人们了解甚少。当前的研究旨在探究铬和镉对瑞士白化小鼠大脑的单独及联合毒性作用,此外还将研究辅酶Q10(CoQ10)、生物chanin-A(BCA)和根皮素(PHL)这三种具有抗氧化特性的天然黄酮类化合物可能的神经保护功能。分别给小鼠口服铬和镉(各75 ppm),同时腹腔注射CoQ10(10 mg/kg)、BCA和PHL(各50 mg/kg)。治疗两周后,进行了一系列生化检测、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作用机制。我们的研究结果强调了本研究的重要性,结果表明,给予这些营养保健品可降低氧化应激,并通过降低丙二醛(MDA)水平和蛋白质羰基含量(PCC),同时提高超氧化物歧化酶(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,从而恢复抗氧化防御系统。还观察到胆碱酯酶活性降低以及组织结构改变。mRNA表达的qRT-PCR分析显示,与抗氧化防御相关的基因(SIRT1、Nrf2、HO-1、NQO1)上调,同时凋亡标志物caspase-8和3分别下调。该研究突出了CoQ10、BCA和PHL通过增强Nrf2介导的外源性抗氧化防御以及减轻细胞损伤和神经细胞凋亡,对铬和镉诱导的氧化应激具有神经保护作用。这些结果表明,这些营养保健品在减轻重金属暴露引起的神经疾病方面可能具有治疗价值,对未来的治疗可能产生重大影响。

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