Salidroside Delays Cellular Senescence by Stimulating Mitochondrial Biogenesis Partly through a miR-22/SIRT-1 Pathway
| العنوان: | Salidroside Delays Cellular Senescence by Stimulating Mitochondrial Biogenesis Partly through a miR-22/SIRT-1 Pathway |
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| المؤلفون: | Gen Xiang Mao, Wen Min Xing, Guo Fu Wang, Zhong Shan Zhang, Xiao Gang Xu, San Ying Wang, Hui Fen Li, Hui Li Su, Jing Yan, Sha Sha Chen, Ya Zhen Wang, Ji Huan Dai, Sean X. Leng, Jing Zhang |
| المصدر: | Oxidative Medicine and Cellular Longevity, Vol 2019 (2019) Oxidative Medicine and Cellular Longevity |
| بيانات النشر: | Hindawi Limited, 2019. |
| سنة النشر: | 2019 |
| مصطلحات موضوعية: | Senescence, Aging, Article Subject, Calorie restriction, Resveratrol, Biochemistry, chemistry.chemical_compound, Glucosides, Phenols, Humans, lcsh:QH573-671, Cellular Senescence, Organelle Biogenesis, biology, lcsh:Cytology, Salidroside, Cell Biology, General Medicine, TFAM, biology.organism_classification, Mitochondria, Cell biology, MicroRNAs, Rhodiola rosea, chemistry, Mitochondrial biogenesis, Rhodiola, Organelle biogenesis, Research Article |
| الوصف: | Calorie restriction (CR) is a nongenetic intervention with a robust effect on delaying aging in mammals and other organisms. A mild stimulation on mitochondrial biogenesis induced by CR seems to be an important action mode for its benefits. Here, we reported that a component isolated from Rhodiola rosea L., salidroside, delays replicative senescence in human fibroblasts, which is related to its stimulation on mitochondrial biogenesis by activating SIRT1 partly resulted from inhibition on miR-22. Salidroside increased the mitochondrial mass that accompanied an increment of the key regulators of mitochondrial biogenesis including PGC-1α, NRF-1, and TFAM and reversed the mitochondrial dysfunction in presenescent 50PD cells, showing a comparable effect to that of resveratrol. SIRT1 is involved in the inducement of mitochondrial biogenesis by salidroside. The declined expression of SIRT1 in 50PD cells compared with the young 30PD cells was prevented upon salidroside treatment. In addition, pretreatment of EX-527, a selective SIRT1 inhibitor, could block the increased mitochondrial mass and decreased ROS production induced by salidroside in 50PD cells, resulting in an accelerated cellular senescence. We further found that salidroside reversed the elevated miR-22 expression in presenescent cells according to a miRNA array analysis and a subsequent qPCR validation. Enforced miR-22 expression by using a Pre-miR-22 lentiviral construct induced the young fibroblasts (30PD) into a senescence state, accompanied with increased senescence-related molecules including p53, p21, p16, and decreased SIRT1 expression, a known target of miR-22. However, salidroside could partly impede the senescence progression induced by lenti-Pre-miR-22. Taken together, our data suggest that salidroside delays replicative senescence by stimulating mitochondrial biogenesis partly through a miR22/SIRT1 pathway, which enriches our current knowledge of a salidroside-mediated postpone senility effect and provides a new perspective on the antidecrepitude function of this naturally occurring compound in animals and humans. |
| وصف الملف: | text/xhtml |
| تدمد: | 1942-0994 1942-0900 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::c40da756ba59497686da2197433d2ed9 https://doi.org/10.1155/2019/5276096 |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....c40da756ba59497686da2197433d2ed9 |
| قاعدة البيانات: | OpenAIRE |
| تدمد: | 19420994 19420900 |
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