揭示辅酶Q10通过靶向PI3K/AKT/Nrf-2信号通路改善大鼠衰老相关的氧化和炎症性肺改变的机制。

IF 2.7 4区 医学 Q3 ENDOCRINOLOGY & METABOLISM
Elshymaa A Abdel-Hakeem, Nisreen D M Toni, Doaa Mohamed Elroby Ali, Heba Marey, Heba A Abdel-Hamid
{"title":"揭示辅酶Q10通过靶向PI3K/AKT/Nrf-2信号通路改善大鼠衰老相关的氧化和炎症性肺改变的机制。","authors":"Elshymaa A Abdel-Hakeem, Nisreen D M Toni, Doaa Mohamed Elroby Ali, Heba Marey, Heba A Abdel-Hamid","doi":"10.1080/13813455.2025.2525415","DOIUrl":null,"url":null,"abstract":"<p><p><b>Objectives</b>: Lung is one of the vital organs that is affected by the ageing process. Searching for natural antioxidants is mandatory to boost healthier longevity. Accordingly, we sought to explore the probable protective effect of Coenzyme Q10 (Q10) on experimentally induced lung ageing and study the supposed involved mechanistic pathways.</p><p><p><b>Methods</b>: Rats were allocated into groups; control, D-galactose (D-gal), D-gal + Q10 and D-gal + Q10+ LY294002 (LY; phosphatidylinositol 3-kinases (PI3K)/protein kinase B (AKT) inhibitor). Sera and lung tissues were gathered for evaluating markers of oxidative stress, inflammation, fibrosis, and cell senescence by different methods.Immunohistochemistry for senescence associated beta galactosidase (SA-βGal), Capsase-3, and P53 were also evaluated.</p><p><p><b>Results</b>: Induction of lung ageing resulted in deleterious lung alterations which were ameliorated by Q10; however, its protective effect was abolished by co-administration of LY.</p><p><p><b>Conclusion</b>: Q10 secured the lung against the ageing process <i>via</i> its antioxidant, anti-inflammatory, and anti-apoptotic effects through the activation of the PI3K/AKT/Nrf-2 pathway.</p>","PeriodicalId":8331,"journal":{"name":"Archives of Physiology and Biochemistry","volume":" ","pages":"1-17"},"PeriodicalIF":2.7000,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Unveiling the mechanism of Coenzyme Q10 in ameliorating ageing related oxidative and inflammatory lung alterations in rats <i>via</i> targeting PI3K/AKT/Nrf-2 signaling pathway.\",\"authors\":\"Elshymaa A Abdel-Hakeem, Nisreen D M Toni, Doaa Mohamed Elroby Ali, Heba Marey, Heba A Abdel-Hamid\",\"doi\":\"10.1080/13813455.2025.2525415\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p><b>Objectives</b>: Lung is one of the vital organs that is affected by the ageing process. Searching for natural antioxidants is mandatory to boost healthier longevity. Accordingly, we sought to explore the probable protective effect of Coenzyme Q10 (Q10) on experimentally induced lung ageing and study the supposed involved mechanistic pathways.</p><p><p><b>Methods</b>: Rats were allocated into groups; control, D-galactose (D-gal), D-gal + Q10 and D-gal + Q10+ LY294002 (LY; phosphatidylinositol 3-kinases (PI3K)/protein kinase B (AKT) inhibitor). Sera and lung tissues were gathered for evaluating markers of oxidative stress, inflammation, fibrosis, and cell senescence by different methods.Immunohistochemistry for senescence associated beta galactosidase (SA-βGal), Capsase-3, and P53 were also evaluated.</p><p><p><b>Results</b>: Induction of lung ageing resulted in deleterious lung alterations which were ameliorated by Q10; however, its protective effect was abolished by co-administration of LY.</p><p><p><b>Conclusion</b>: Q10 secured the lung against the ageing process <i>via</i> its antioxidant, anti-inflammatory, and anti-apoptotic effects through the activation of the PI3K/AKT/Nrf-2 pathway.</p>\",\"PeriodicalId\":8331,\"journal\":{\"name\":\"Archives of Physiology and Biochemistry\",\"volume\":\" \",\"pages\":\"1-17\"},\"PeriodicalIF\":2.7000,\"publicationDate\":\"2025-07-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Archives of Physiology and Biochemistry\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1080/13813455.2025.2525415\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"ENDOCRINOLOGY & METABOLISM\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Archives of Physiology and Biochemistry","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/13813455.2025.2525415","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"ENDOCRINOLOGY & METABOLISM","Score":null,"Total":0}
引用次数: 0

摘要

目的:肺是受衰老影响的重要器官之一。寻找天然抗氧化剂是促进健康长寿的必要条件。因此,我们试图探索辅酶Q10 (Q10)对实验诱导的肺衰老的可能保护作用,并研究可能涉及的机制途径。方法:将大鼠分为两组;对照,d -半乳糖(D-gal), D-gal + Q10和D-gal + Q10+ LY294002 (LY;磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B (AKT)抑制剂)。收集血清和肺组织,用不同的方法评估氧化应激、炎症、纤维化和细胞衰老的标志物。免疫组化检测衰老相关的β -半乳糖苷酶(SA-βGal)、capase -3和P53。结果:诱导肺老化导致有害的肺改变,Q10可改善这种改变;然而,它的保护作用被联合给药LY所消除。结论:Q10通过激活PI3K/AKT/Nrf-2通路,具有抗氧化、抗炎和抗凋亡作用,从而保护肺部免受衰老过程的影响。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Unveiling the mechanism of Coenzyme Q10 in ameliorating ageing related oxidative and inflammatory lung alterations in rats via targeting PI3K/AKT/Nrf-2 signaling pathway.

Objectives: Lung is one of the vital organs that is affected by the ageing process. Searching for natural antioxidants is mandatory to boost healthier longevity. Accordingly, we sought to explore the probable protective effect of Coenzyme Q10 (Q10) on experimentally induced lung ageing and study the supposed involved mechanistic pathways.

Methods: Rats were allocated into groups; control, D-galactose (D-gal), D-gal + Q10 and D-gal + Q10+ LY294002 (LY; phosphatidylinositol 3-kinases (PI3K)/protein kinase B (AKT) inhibitor). Sera and lung tissues were gathered for evaluating markers of oxidative stress, inflammation, fibrosis, and cell senescence by different methods.Immunohistochemistry for senescence associated beta galactosidase (SA-βGal), Capsase-3, and P53 were also evaluated.

Results: Induction of lung ageing resulted in deleterious lung alterations which were ameliorated by Q10; however, its protective effect was abolished by co-administration of LY.

Conclusion: Q10 secured the lung against the ageing process via its antioxidant, anti-inflammatory, and anti-apoptotic effects through the activation of the PI3K/AKT/Nrf-2 pathway.

求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
来源期刊
Archives of Physiology and Biochemistry
Archives of Physiology and Biochemistry ENDOCRINOLOGY & METABOLISM-PHYSIOLOGY
CiteScore
6.90
自引率
3.30%
发文量
21
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.
×
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