Effects of Vitamin D on Lumbar Disk Degeneration Based on PINK1/Parkin Signaling Pathway

IF 0.4 4区 医学 Q4 NUTRITION & DIETETICS
Zhe Shen, Tao Lan, Weizhuang Guo
{"title":"Effects of Vitamin D on Lumbar Disk Degeneration Based on PINK1/Parkin Signaling Pathway","authors":"Zhe Shen, Tao Lan, Weizhuang Guo","doi":"10.37290/ctnr2641-452x.22:237-245","DOIUrl":null,"url":null,"abstract":"Vitamin D affects calcium homeostasis and is a crucial factor in cytoplasmic and mitochondrial interactions implicated in muscle energy metabolism. This study probed the effect of vitamin D on lumbar disk degeneration based on the PINK1/Parkin signaling pathway. Primary nucleus pulposus cells from Sprague-Dawley rats were cultured to construct a model of oxidative stress in vitro, and the expression and activity of target proteins in related genes and signaling pathways were detected via real-time quantitative polymerase chain reaction and western blotting. We simulated disk degeneration by inducing high levels of oxidative stress in nucleus pulposus cells with 100 μM hydrogen peroxide. Vitamin D treatment could effectively increase the expression of genes related to the nucleus pulposus matrix as well as decrease disk degeneration factors’ expression. Further mechanism results displayed that vitamin D effectively reduced oxidative stress indexes in nucleus pulposus cell s and alleviated hydrogen peroxide-mediated degeneration of nucleus pulposus cells by activating the PINK1/Parkin pathway. We confirm that vitamin D activates the PINK1/Parkin pathway to play an antioxidative stress role and delay the aging and degeneration of nucleus pulposus cells.","PeriodicalId":10976,"journal":{"name":"Current Topics in Nutraceutical Research","volume":"22 1","pages":"237-245"},"PeriodicalIF":0.4000,"publicationDate":"2023-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Topics in Nutraceutical Research","FirstCategoryId":"0","ListUrlMain":"https://doi.org/10.37290/ctnr2641-452x.22:237-245","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"NUTRITION & DIETETICS","Score":null,"Total":0}
引用次数: 0

Abstract

Vitamin D affects calcium homeostasis and is a crucial factor in cytoplasmic and mitochondrial interactions implicated in muscle energy metabolism. This study probed the effect of vitamin D on lumbar disk degeneration based on the PINK1/Parkin signaling pathway. Primary nucleus pulposus cells from Sprague-Dawley rats were cultured to construct a model of oxidative stress in vitro, and the expression and activity of target proteins in related genes and signaling pathways were detected via real-time quantitative polymerase chain reaction and western blotting. We simulated disk degeneration by inducing high levels of oxidative stress in nucleus pulposus cells with 100 μM hydrogen peroxide. Vitamin D treatment could effectively increase the expression of genes related to the nucleus pulposus matrix as well as decrease disk degeneration factors’ expression. Further mechanism results displayed that vitamin D effectively reduced oxidative stress indexes in nucleus pulposus cell s and alleviated hydrogen peroxide-mediated degeneration of nucleus pulposus cells by activating the PINK1/Parkin pathway. We confirm that vitamin D activates the PINK1/Parkin pathway to play an antioxidative stress role and delay the aging and degeneration of nucleus pulposus cells.
基于PINK1/Parkin信号通路的维生素D对腰椎间盘退变的影响
维生素D影响钙稳态,是细胞质和线粒体相互作用中涉及肌肉能量代谢的关键因素。本研究基于PINK1/Parkin信号通路探讨维生素D对腰椎间盘退变的影响。体外培养Sprague-Dawley大鼠原代髓核细胞构建氧化应激模型,采用实时定量聚合酶链反应和western blotting检测相关基因和信号通路中靶蛋白的表达和活性。我们用100 μM过氧化氢诱导髓核细胞高水平氧化应激,模拟椎间盘退变。维生素D处理能有效提高髓核基质相关基因的表达,降低椎间盘退变因子的表达。进一步的机制研究表明,维生素D通过激活PINK1/Parkin通路,有效降低髓核细胞氧化应激指标,减轻过氧化氢介导的髓核细胞变性。我们证实维生素D激活PINK1/Parkin通路,发挥抗氧化应激作用,延缓髓核细胞的衰老和变性。
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
CiteScore
1.10
自引率
0.00%
发文量
36
审稿时长
>12 weeks
期刊介绍: Current Topics in Nutraceutical Research is an international, interdisciplinary broad-based peer reviewed scientific journal for critical evaluation of research on chemistry, biology and therapeutic applications of nutraceuticals and functional foods. The major goal of this journal is to provide peer reviewed unbiased scientific data to the decision makers in the nutraceutical and food industry to help make informed choices about development of new products. To this end, the journal will publish two types of review articles. First, a review of preclinical research data coming largely from animal, cell culture and other experimental models. Such data will provide basis for future product development and/or human research initiatives. Second, a critical evaluation of current human experimental data to help market and deliver the product for medically proven use. This journal will also serve as a forum for nutritionists, internists, neurologists, psychiatrists, and all those interested in preventive medicine. The common denominator of all of the topic to be covered by the journal must include nutraceuticals and/functional food. The following is an example of some specific areas that may be of interest to the journal. i) Role of vitamins, minerals, antioxidants and phytonutrients on cardiovascular health, cancer, diabetes, ocular health, mental health, men’s health, women’s health, infant nutrition, ii) Role of herbals on human health, iii) Dietary supplements and sleep, iv) Components of diet that may have beneficial effect on human health, v) regulation of apoptosis and cell viability, vi) Isolation and characterization of bioactive components from functional foods, vii) Nutritional genomics, and viii) Nutritional proteomics.
×
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:604180095
Book学术官方微信
小红书