Salidroside Delays Cellular Senescence by Stimulating Mitochondrial Biogenesis Partly through a MIR-22/SIRT-1 Pathway

Gen Xiang Mao, Xiao Gang Xu, San Ying Wang, Huifen Li, Jing Zhang, Zhong Shan Zhang, Hui Li Su, Sha Sha Chen, Wen Min Xing, Ya Zhen Wang, Ji Huan Dai, Guo Fu Wang, Sean Leng, Jing Yan

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Article number5276096
JournalOxidative medicine and cellular longevity
Volume2019
DOIs
StatePublished - Jan 1 2019

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Mammals
Cell Aging
Polymerase chain reaction
Biosynthesis
Organelle Biogenesis
Fibroblasts
RNA
Cell culture
Cell Culture Techniques
Resveratrol
Polymerase Chain Reaction
Animals
Aging of materials
Molecules
Rhodiola
rhodioloside
MicroRNAs

ASJC Scopus subject areas

  • Biochemistry
  • Aging
  • Cell Biology

Cite this

Salidroside Delays Cellular Senescence by Stimulating Mitochondrial Biogenesis Partly through a MIR-22/SIRT-1 Pathway. / Mao, Gen Xiang; Xu, Xiao Gang; Wang, San Ying; Li, Huifen; Zhang, Jing; Zhang, Zhong Shan; Su, Hui Li; Chen, Sha Sha; Xing, Wen Min; Wang, Ya Zhen; Dai, Ji Huan; Wang, Guo Fu; Leng, Sean; Yan, Jing.

In: Oxidative medicine and cellular longevity, Vol. 2019, 5276096, 01.01.2019.

Research output: Contribution to journalArticle

Mao, GX, Xu, XG, Wang, SY, Li, H, Zhang, J, Zhang, ZS, Su, HL, Chen, SS, Xing, WM, Wang, YZ, Dai, JH, Wang, GF, Leng, S & Yan, J 2019, 'Salidroside Delays Cellular Senescence by Stimulating Mitochondrial Biogenesis Partly through a MIR-22/SIRT-1 Pathway', Oxidative medicine and cellular longevity, vol. 2019, 5276096. https://doi.org/10.1155/2019/5276096
Mao, Gen Xiang ; Xu, Xiao Gang ; Wang, San Ying ; Li, Huifen ; Zhang, Jing ; Zhang, Zhong Shan ; Su, Hui Li ; Chen, Sha Sha ; Xing, Wen Min ; Wang, Ya Zhen ; Dai, Ji Huan ; Wang, Guo Fu ; Leng, Sean ; Yan, Jing. / Salidroside Delays Cellular Senescence by Stimulating Mitochondrial Biogenesis Partly through a MIR-22/SIRT-1 Pathway. In: Oxidative medicine and cellular longevity. 2019 ; Vol. 2019.
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abstract = "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.",
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AU - Mao, Gen Xiang

AU - Xu, Xiao Gang

AU - Wang, San Ying

AU - Li, Huifen

AU - Zhang, Jing

AU - Zhang, Zhong Shan

AU - Su, Hui Li

AU - Chen, Sha Sha

AU - Xing, Wen Min

AU - Wang, Ya Zhen

AU - Dai, Ji Huan

AU - Wang, Guo Fu

AU - Leng, Sean

AU - Yan, Jing

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N2 - 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.

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