Rutin Attenuates Pirarubicin-Induced Cardiomyocyte Injury by Knocking Down lncRNA Miat

IF 2.8 3区医学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Journal of Biochemical and Molecular Toxicology Pub Date : 2025-01-26 DOI:10.1002/jbt.70144

Peng Huang, Kaixu Yan, Wenqing Zhang, Jiahua Ji, Dexian Wei, Wentao Zheng, Lu Li, Liqun Ren

{"title":"Rutin Attenuates Pirarubicin-Induced Cardiomyocyte Injury by Knocking Down lncRNA Miat","authors":"Peng Huang, Kaixu Yan, Wenqing Zhang, Jiahua Ji, Dexian Wei, Wentao Zheng, Lu Li, Liqun Ren","doi":"10.1002/jbt.70144","DOIUrl":null,"url":null,"abstract":"<div>\n \n <p>Pirarubicin (THP) is a widely used chemotherapeutic agent for breast cancer, but its clinical use is limited by its cardiotoxicity. In our previous study, we found that rutin (RUT), the main active ingredient in the traditional Chinese medicine Sophora japonica, could attenuate THP-induced cardiotoxicity. The aim of this study was to further investigate the potential role and mechanism of RUT in attenuating THP-induced cardiotoxicity. We examined the expression of lncRNA Miat in mouse cardiomyocytes (HL-1) under the intervention of THP/THP + RUT, respectively. Then we evaluated the protective effect of RUT on THP-induced HL-1 by CCK8, TUNEL, reactive oxygen species (ROS) assay and Western Blot. The mediating role of lncRNA Miat was verified by transfection of overexpression lncRNA Miat plasmid. The results showed that RUT increased cell viability, inhibited apoptosis, reduced ROS accumulation and decreased calcium overload in THP-induced HL-1. While overexpression of Miat significantly abrogated the therapeutic effect of rutin. In conclusion, RUT attenuates THP-induced myocardial injury by downregulating lncRNA Miat.</p></div>","PeriodicalId":15151,"journal":{"name":"Journal of Biochemical and Molecular Toxicology","volume":"39 2","pages":""},"PeriodicalIF":2.8000,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Biochemical and Molecular Toxicology","FirstCategoryId":"3","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jbt.70144","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}

引用次数: 0

Abstract

Pirarubicin (THP) is a widely used chemotherapeutic agent for breast cancer, but its clinical use is limited by its cardiotoxicity. In our previous study, we found that rutin (RUT), the main active ingredient in the traditional Chinese medicine Sophora japonica, could attenuate THP-induced cardiotoxicity. The aim of this study was to further investigate the potential role and mechanism of RUT in attenuating THP-induced cardiotoxicity. We examined the expression of lncRNA Miat in mouse cardiomyocytes (HL-1) under the intervention of THP/THP + RUT, respectively. Then we evaluated the protective effect of RUT on THP-induced HL-1 by CCK8, TUNEL, reactive oxygen species (ROS) assay and Western Blot. The mediating role of lncRNA Miat was verified by transfection of overexpression lncRNA Miat plasmid. The results showed that RUT increased cell viability, inhibited apoptosis, reduced ROS accumulation and decreased calcium overload in THP-induced HL-1. While overexpression of Miat significantly abrogated the therapeutic effect of rutin. In conclusion, RUT attenuates THP-induced myocardial injury by downregulating lncRNA Miat.

Abstract Image

查看原文

微信好友朋友圈 QQ好友复制链接

本刊更多论文

芦丁通过下调lncRNA Miat减轻吡柔比星诱导的心肌细胞损伤

吡柔比星（THP）是一种广泛应用于乳腺癌的化疗药物，但其心脏毒性限制了其临床应用。在我们之前的研究中，我们发现中药苦参的主要活性成分芦丁（rutin， RUT）可以减弱thp引起的心脏毒性。本研究旨在进一步探讨RUT在减轻thp诱导的心脏毒性中的潜在作用和机制。我们分别检测了THP/THP + RUT干预下小鼠心肌细胞（HL-1）中lncRNA Miat的表达。然后采用CCK8、TUNEL、活性氧（ROS）检测和Western Blot检测RUT对thp诱导的HL-1的保护作用。转染过表达lncRNA Miat质粒，验证lncRNA Miat的介导作用。结果表明，RUT可提高thp诱导的HL-1细胞活力，抑制细胞凋亡，减少ROS积累，降低钙超载。而Miat的过表达明显抵消了芦丁的治疗效果。综上所述，RUT通过下调lncRNA Miat来减轻thp诱导的心肌损伤。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

求助全文

约1分钟内获得全文去求助

来源期刊

Journal of Biochemical and Molecular Toxicology 生物-毒理学

CiteScore

5.80

自引率

2.80%

发文量

277

审稿时长

6-12 weeks

期刊介绍： The Journal of Biochemical and Molecular Toxicology is an international journal that contains original research papers, rapid communications, mini-reviews, and book reviews, all focusing on the molecular mechanisms of action and detoxication of exogenous and endogenous chemicals and toxic agents. The scope includes effects on the organism at all stages of development, on organ systems, tissues, and cells as well as on enzymes, receptors, hormones, and genes. The biochemical and molecular aspects of uptake, transport, storage, excretion, lactivation and detoxication of drugs, agricultural, industrial and environmental chemicals, natural products and food additives are all subjects suitable for publication. Of particular interest are aspects of molecular biology related to biochemical toxicology. These include studies of the expression of genes related to detoxication and activation enzymes, toxicants with modes of action involving effects on nucleic acids, gene expression and protein synthesis, and the toxicity of products derived from biotechnology.