Vitamin D Protects Against Cardiac Hypertrophy Through the Regulation of Mitochondrial Function in Aging Rats.

Rejuvenation research Pub Date : 2024-04-01 Epub Date: 2024-02-20 DOI:10.1089/rej.2023.0061
Siamak Shahidi, Alireza Komaki, Iraj Salehi, Sara Soleimani Asl, Parisa Habibi, Fatemeh Ramezani-Aliakbari
{"title":"Vitamin D Protects Against Cardiac Hypertrophy Through the Regulation of Mitochondrial Function in Aging Rats.","authors":"Siamak Shahidi, Alireza Komaki, Iraj Salehi, Sara Soleimani Asl, Parisa Habibi, Fatemeh Ramezani-Aliakbari","doi":"10.1089/rej.2023.0061","DOIUrl":null,"url":null,"abstract":"<p><p>Cardiac aging is defined as mitochondrial dysfunction of the heart. Vitamin D (VitD) is an effective agent in ameliorating cardiovascular disorders. In this study, we indicated the protective effects of VitD against cardiac aging. Male Wistar rats were randomly divided into four groups: control (CONT), D-galactose (D-GAL): aged rats induced by D-GAL, D-GAL + Ethanol: aged rats treated with ethanol, and D-GAL + VitD aged rats treated with VitD. Aging was induced by D-GAL at 150 mg/kg via intraperitoneal injection for 8 weeks. Aged rats were treated with VitD (D-GAL + VitD) by gavage for 8 weeks. The serum samples were used to evaluate biochemical factors, and heart tissues were assessed to determine oxidative stress and gene expression. The D-GAL rats exhibited cardiac hypertrophy, which was associated with decreased antioxidant enzyme activity, enhanced oxidative marker, and changes in the expression of mitochondrial genes in comparison with the control rats. Co-treatment with VitD ameliorated all these changes. In conclusion, VitD could protect the heart against D-GAL-induced aging via enhancin<i>g</i> antioxidant effects, and the expression of mitochondrial genes.</p>","PeriodicalId":94189,"journal":{"name":"Rejuvenation research","volume":" ","pages":"51-60"},"PeriodicalIF":0.0000,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Rejuvenation research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1089/rej.2023.0061","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/2/20 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0

Abstract

Cardiac aging is defined as mitochondrial dysfunction of the heart. Vitamin D (VitD) is an effective agent in ameliorating cardiovascular disorders. In this study, we indicated the protective effects of VitD against cardiac aging. Male Wistar rats were randomly divided into four groups: control (CONT), D-galactose (D-GAL): aged rats induced by D-GAL, D-GAL + Ethanol: aged rats treated with ethanol, and D-GAL + VitD aged rats treated with VitD. Aging was induced by D-GAL at 150 mg/kg via intraperitoneal injection for 8 weeks. Aged rats were treated with VitD (D-GAL + VitD) by gavage for 8 weeks. The serum samples were used to evaluate biochemical factors, and heart tissues were assessed to determine oxidative stress and gene expression. The D-GAL rats exhibited cardiac hypertrophy, which was associated with decreased antioxidant enzyme activity, enhanced oxidative marker, and changes in the expression of mitochondrial genes in comparison with the control rats. Co-treatment with VitD ameliorated all these changes. In conclusion, VitD could protect the heart against D-GAL-induced aging via enhancing antioxidant effects, and the expression of mitochondrial genes.

维生素 D 通过调节衰老大鼠的线粒体功能防止心肌肥大。
心脏衰老是指心脏线粒体功能障碍。维生素 D(VitD)是改善心血管疾病的有效药物。在这项研究中,我们指出了维生素 D 对心脏衰老的保护作用。雄性 Wistar 大鼠被随机分为四组:对照组(CONT)、D-半乳糖组(D-GAL):由 D-半乳糖(D-GAL)诱导的衰老大鼠、D-GAL+乙醇组:用乙醇治疗的衰老大鼠,以及 D-GAL+ VitD 组:用 VitD 治疗的衰老大鼠。通过腹腔注射 150 毫克/千克的 D-GAL 诱导衰老,持续八周。给老年大鼠灌胃 VitD(D-GAL+ VitD)治疗八周。血清样本用于评估生化因子,心脏组织用于评估氧化应激和基因表达。与对照组大鼠相比,D-GAL 大鼠表现出心脏肥大,与抗氧化酶活性降低、氧化标记物增强和线粒体基因表达变化有关。与对照组大鼠相比,VitD 可改善所有这些变化。总之,VitD可通过增强抗氧化作用和线粒体基因的表达,保护心脏免受D-GAL诱导的衰老。
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 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信