Rapamycin mitigates erythrocyte membrane transport functions and oxidative stress during aging in rats.

IF 2.5 4区医学 Q3 ENDOCRINOLOGY & METABOLISM

Archives of Physiology and Biochemistry Pub Date : 2018-02-01 Epub Date: 2017-07-31 DOI:10.1080/13813455.2017.1359629

Abhishek Kumar Singh, Sandeep Singh, Geetika Garg, Syed Ibrahim Rizvi

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引用次数: 17

Abstract

Erythrocyte membrane is a suitable model to study various metabolic and physiological functions as it undergoes variety of biochemical changes during aging. An age-dependent modulatory effect of rapamycin on erythrocyte membrane functions is completely unknown. Therefore, the present study was undertaken to investigate the effect of rapamycin on age-dependent impaired activities of transporters/exchangers, altered levels of redox biomarkers, viz. protein carbonyl (PC), lipid hydroperoxides (LHs), total thiol (-SH), sialic acid (SA) and intracellular calcium ion [Ca²⁺]i, and osmotic fragility of erythrocyte membrane. A significant reduction in membrane-bound activities of Na⁺/K⁺-ATPase (NKA) and Ca²⁺-ATPase (PMCA), and levels of -SH and SA was observed along with a simultaneous induction in Na⁺/H⁺ exchanger (NHE) activity and levels of [Ca²⁺]i, PC, LH and osmotic fragility in old-aged rats. Rapamycin was found to be a promising age-delaying drug that significantly reversed the aging-induced impaired activities of membrane-bound ATPases and altered levels of redox biomarkers.

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雷帕霉素减轻大鼠衰老过程中红细胞膜转运功能和氧化应激。

红细胞膜在衰老过程中经历了多种生化变化，是研究各种代谢和生理功能的合适模型。雷帕霉素对红细胞膜功能的年龄依赖性调节作用是完全未知的。因此，本研究旨在探讨雷帕霉素对转运体/交换体的年龄依赖性活性受损、氧化还原生物标志物(即蛋白质羰基(PC)、脂质氢过氧化物(LHs)、总硫醇(-SH)、唾液酸(SA)和细胞内钙离子[Ca2+]i)水平的改变以及红细胞膜渗透脆弱性的影响。在老龄大鼠中，Na+/K+- atp酶(NKA)和Ca2+- atp酶(PMCA)的膜结合活性以及-SH和SA水平显著降低，同时Na+/H+交换剂(NHE)活性和[Ca2+]i、PC、LH和渗透脆性水平也显著降低。雷帕霉素被发现是一种很有前景的延缓衰老药物，可以显著逆转衰老引起的膜结合atp酶活性受损和氧化还原生物标志物水平的改变。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY

CiteScore

6.90

自引率

3.30%

发文量

期刊介绍： Archives of Physiology and Biochemistry: The Journal of Metabolic Diseases is an international peer-reviewed journal which has been relaunched to meet the increasing demand for integrated publication on molecular, biochemical and cellular aspects of metabolic diseases, as well as clinical and therapeutic strategies for their treatment. It publishes full-length original articles, rapid papers, reviews and mini-reviews on selected topics. It is the overall goal of the journal to disseminate novel approaches to an improved understanding of major metabolic disorders. The scope encompasses all topics related to the molecular and cellular pathophysiology of metabolic diseases like obesity, type 2 diabetes and the metabolic syndrome, and their associated complications. Clinical studies are considered as an integral part of the Journal and should be related to one of the following topics: -Dysregulation of hormone receptors and signal transduction -Contribution of gene variants and gene regulatory processes -Impairment of intermediary metabolism at the cellular level -Secretion and metabolism of peptides and other factors that mediate cellular crosstalk -Therapeutic strategies for managing metabolic diseases Special issues dedicated to topics in the field will be published regularly.