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Resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ROS-mediated PI3K/Akt pathway

Background: Diabetes mellitus is closely correlated with disc degeneration. Nucleus pulposus (NP) cell apoptosis and senescence are typical cellular features within the degenerative disc. Resveratrol is a newly identified phytoalexin that has protective effects on cartilaginous tissue. Objective: To...

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Autores principales: Wang, Wenping, Li, Pei, Xu, Jiagang, Wu, Xiangkun, Guo, Zhiliang, Fan, Lijing, Song, Ruipeng, Wang, Jianli, Wei, Li, Teng, Haijun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5897744/
https://www.ncbi.nlm.nih.gov/pubmed/29273676
http://dx.doi.org/10.1042/BSR20171454
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author Wang, Wenping
Li, Pei
Xu, Jiagang
Wu, Xiangkun
Guo, Zhiliang
Fan, Lijing
Song, Ruipeng
Wang, Jianli
Wei, Li
Teng, Haijun
author_facet Wang, Wenping
Li, Pei
Xu, Jiagang
Wu, Xiangkun
Guo, Zhiliang
Fan, Lijing
Song, Ruipeng
Wang, Jianli
Wei, Li
Teng, Haijun
author_sort Wang, Wenping
collection PubMed
description Background: Diabetes mellitus is closely correlated with disc degeneration. Nucleus pulposus (NP) cell apoptosis and senescence are typical cellular features within the degenerative disc. Resveratrol is a newly identified phytoalexin that has protective effects on cartilaginous tissue. Objective: To investigate the whether resveratrol can protect against high glucose-induced NP cell apoptosis and senescence, and the potential mechanism in this process. Methods: Rat NP cells were cultured in either 10% FBS culture medium (control group) or 10% FBS with a high glucose concentration (0.2 M, experiment group) for 3 days. Resveratrol or the combination of resveratrol and LY294002 was added into the culture medium of experiment group to investigate the effects of resveratrol and the PI3K/Akt pathway. Results: High glucose significantly promoted NP cell apoptosis and NP cell senescence compared with the control group. Resveratrol exhibited protective effects against high glucose-induced NP cell apoptosis and senescence. Further analysis showed that resveratrol suppressed reactive oxygen species (ROS) generation and increased the activity of the PI3K/Akt pathway under the high glucose condition. However, the LY294002 had no significant effects on ROS content in the resveratrol-treated high glucose group. Conclusion: Resveratrol can attenuate high glucose-induced NP cell apoptosis and senescence, and the activation of ROS-mediated PI3K/Akt pathway may be the potential mechanism in this process.
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spelling pubmed-58977442018-04-17 Resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ROS-mediated PI3K/Akt pathway Wang, Wenping Li, Pei Xu, Jiagang Wu, Xiangkun Guo, Zhiliang Fan, Lijing Song, Ruipeng Wang, Jianli Wei, Li Teng, Haijun Biosci Rep Research Articles Background: Diabetes mellitus is closely correlated with disc degeneration. Nucleus pulposus (NP) cell apoptosis and senescence are typical cellular features within the degenerative disc. Resveratrol is a newly identified phytoalexin that has protective effects on cartilaginous tissue. Objective: To investigate the whether resveratrol can protect against high glucose-induced NP cell apoptosis and senescence, and the potential mechanism in this process. Methods: Rat NP cells were cultured in either 10% FBS culture medium (control group) or 10% FBS with a high glucose concentration (0.2 M, experiment group) for 3 days. Resveratrol or the combination of resveratrol and LY294002 was added into the culture medium of experiment group to investigate the effects of resveratrol and the PI3K/Akt pathway. Results: High glucose significantly promoted NP cell apoptosis and NP cell senescence compared with the control group. Resveratrol exhibited protective effects against high glucose-induced NP cell apoptosis and senescence. Further analysis showed that resveratrol suppressed reactive oxygen species (ROS) generation and increased the activity of the PI3K/Akt pathway under the high glucose condition. However, the LY294002 had no significant effects on ROS content in the resveratrol-treated high glucose group. Conclusion: Resveratrol can attenuate high glucose-induced NP cell apoptosis and senescence, and the activation of ROS-mediated PI3K/Akt pathway may be the potential mechanism in this process. Portland Press Ltd. 2018-04-13 /pmc/articles/PMC5897744/ /pubmed/29273676 http://dx.doi.org/10.1042/BSR20171454 Text en © 2018 The Author(s). http://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (http://creativecommons.org/licenses/by/4.0/) .
spellingShingle Research Articles
Wang, Wenping
Li, Pei
Xu, Jiagang
Wu, Xiangkun
Guo, Zhiliang
Fan, Lijing
Song, Ruipeng
Wang, Jianli
Wei, Li
Teng, Haijun
Resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ROS-mediated PI3K/Akt pathway
title Resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ROS-mediated PI3K/Akt pathway
title_full Resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ROS-mediated PI3K/Akt pathway
title_fullStr Resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ROS-mediated PI3K/Akt pathway
title_full_unstemmed Resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ROS-mediated PI3K/Akt pathway
title_short Resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ROS-mediated PI3K/Akt pathway
title_sort resveratrol attenuates high glucose-induced nucleus pulposus cell apoptosis and senescence through activating the ros-mediated pi3k/akt pathway
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5897744/
https://www.ncbi.nlm.nih.gov/pubmed/29273676
http://dx.doi.org/10.1042/BSR20171454
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