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}
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.
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.