Salicin prevents TNF-α-induced cellular senescence in human umbilical vein endothelial cells (HUVECs)
Cellular senescence is strongly tied to vascular disease. The current study aims to examine ways that endothelial cellular senescence can be prevented and the mechanisms by which prevention of senescence occurs. Human umbilical vein endothelial cells were exposed to TNF-α to induce senescence; then...
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2019-12-01
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| Series: | Artificial Cells, Nanomedicine, and Biotechnology |
| Subjects: | |
| Online Access: | https://www.tandfonline.com/doi/10.1080/21691401.2019.1629949 |
| _version_ | 1818140634637139968 |
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| author | Fei Guo Rong Wu Jian Xu |
| author_facet | Fei Guo Rong Wu Jian Xu |
| author_sort | Fei Guo |
| collection | DOAJ |
| description | Cellular senescence is strongly tied to vascular disease. The current study aims to examine ways that endothelial cellular senescence can be prevented and the mechanisms by which prevention of senescence occurs. Human umbilical vein endothelial cells were exposed to TNF-α to induce senescence; then salicin was administered in two doses – 50 and 100 µM – to establish a dose-dependent effect of salicin on SA-β-Gal, G1 cell cycle arrest, expression of p21 and PAI-1, p53 acetylation at K382, NRF2 and oxidative stress. NRF2 was examined as a mediating mechanism of salicin’s impact on cellular senescence and was found to account for salicin’s impact on SA-β-Gal, p21, PAI-1 and p53. Together, these results provide a compelling case that salicin has a substantial impact on numerous factors tied to cellular senescence in human endothelial cells. Thus, treatment with salicin may hold promise as a means of preventing aging-related vascular disease. Furthermore, salicin appears to operate via a functional pathway that is different from that affected by anti-inflammatory drugs (e.g. aspirin). |
| first_indexed | 2024-12-11T10:47:06Z |
| format | Article |
| id | doaj.art-454e9a9c25ca46a28162f83cc7f24113 |
| institution | Directory Open Access Journal |
| issn | 2169-1401 2169-141X |
| language | English |
| last_indexed | 2024-12-11T10:47:06Z |
| publishDate | 2019-12-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Artificial Cells, Nanomedicine, and Biotechnology |
| spelling | doaj.art-454e9a9c25ca46a28162f83cc7f241132022-12-22T01:10:26ZengTaylor & Francis GroupArtificial Cells, Nanomedicine, and Biotechnology2169-14012169-141X2019-12-014712618262310.1080/21691401.2019.1629949Salicin prevents TNF-α-induced cellular senescence in human umbilical vein endothelial cells (HUVECs)Fei Guo0Rong Wu1Jian Xu2Department of Cardiology, the Provincial Hospital Affiliated to Anhui Medical University, Hefei, P. R. ChinaDepartment of Reproduction, First Affiliated Hospital of Medical University of Anhui, Hefei, P. R. ChinaDepartment of Cardiology, the Provincial Hospital Affiliated to Anhui Medical University, Hefei, P. R. ChinaCellular senescence is strongly tied to vascular disease. The current study aims to examine ways that endothelial cellular senescence can be prevented and the mechanisms by which prevention of senescence occurs. Human umbilical vein endothelial cells were exposed to TNF-α to induce senescence; then salicin was administered in two doses – 50 and 100 µM – to establish a dose-dependent effect of salicin on SA-β-Gal, G1 cell cycle arrest, expression of p21 and PAI-1, p53 acetylation at K382, NRF2 and oxidative stress. NRF2 was examined as a mediating mechanism of salicin’s impact on cellular senescence and was found to account for salicin’s impact on SA-β-Gal, p21, PAI-1 and p53. Together, these results provide a compelling case that salicin has a substantial impact on numerous factors tied to cellular senescence in human endothelial cells. Thus, treatment with salicin may hold promise as a means of preventing aging-related vascular disease. Furthermore, salicin appears to operate via a functional pathway that is different from that affected by anti-inflammatory drugs (e.g. aspirin).https://www.tandfonline.com/doi/10.1080/21691401.2019.1629949Salicinendothelial dysfunctioncell senescenceTNF-αHUVECsSASP |
| spellingShingle | Fei Guo Rong Wu Jian Xu Salicin prevents TNF-α-induced cellular senescence in human umbilical vein endothelial cells (HUVECs) Artificial Cells, Nanomedicine, and Biotechnology Salicin endothelial dysfunction cell senescence TNF-α HUVECs SASP |
| title | Salicin prevents TNF-α-induced cellular senescence in human umbilical vein endothelial cells (HUVECs) |
| title_full | Salicin prevents TNF-α-induced cellular senescence in human umbilical vein endothelial cells (HUVECs) |
| title_fullStr | Salicin prevents TNF-α-induced cellular senescence in human umbilical vein endothelial cells (HUVECs) |
| title_full_unstemmed | Salicin prevents TNF-α-induced cellular senescence in human umbilical vein endothelial cells (HUVECs) |
| title_short | Salicin prevents TNF-α-induced cellular senescence in human umbilical vein endothelial cells (HUVECs) |
| title_sort | salicin prevents tnf α induced cellular senescence in human umbilical vein endothelial cells huvecs |
| topic | Salicin endothelial dysfunction cell senescence TNF-α HUVECs SASP |
| url | https://www.tandfonline.com/doi/10.1080/21691401.2019.1629949 |
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