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The protective effect of propofol on ionizing radiation-induced hematopoietic system damage in mice
The hematopoietic system is highly sensitive to ionizing radiation (IR), and IR can cause injury to hematopoietic stem cells (HSCs); the main reason for this may be elevated reactive oxygen species (ROS) levels. Propofol is an anesthetic drug commonly used in clinical practice. The chemical structur...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Royal Society of Chemistry
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9075036/ https://www.ncbi.nlm.nih.gov/pubmed/35540614 http://dx.doi.org/10.1039/c9ra07262d |
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author | Han, Xiaoliang Sun, Fengtao Zhang, Ying Wang, Jinyan Liu, Qingguo Gao, Ping Zhang, Shubo |
author_facet | Han, Xiaoliang Sun, Fengtao Zhang, Ying Wang, Jinyan Liu, Qingguo Gao, Ping Zhang, Shubo |
author_sort | Han, Xiaoliang |
collection | PubMed |
description | The hematopoietic system is highly sensitive to ionizing radiation (IR), and IR can cause injury to hematopoietic stem cells (HSCs); the main reason for this may be elevated reactive oxygen species (ROS) levels. Propofol is an anesthetic drug commonly used in clinical practice. The chemical structure of propofol is similar to that of vitamin E, and propofol has an antioxidant capacity. Therefore, in this work the effect of using propofol to protect against IR-induced hematopoietic system injury is evaluated. The data suggested that when the irradiated mice were treated with 20 mg kg(−1) of propofol, the survival rate of lethally irradiated mice increased significantly, furthermore, the radiation-induced decrease of white blood cells (WBCs), red blood cells (RBCs), hemoglobin (HGC) and platelets (PLT) in peripheral blood is improved significantly. In addition, propofol could also increase the irradiated HSC and hematopoietic progenitor cell (HPC) frequencies, improving the self-renewal and differentiation abilities of HSCs and HPCs in irradiated mice. Next the ROS levels in HSCs and HPCs were measured, and the results showed that propofol could effectively decrease the ROS levels in these cells. The underlying ROS-scavenging mechanisms are further explored, and the results show that the Nrf2 pathway plays an important role in propofol's radiation protective effects, however, propofol can also increase the proliferation of the Nrf2 inhibitor-treated Lineage(−) cells after exposure to 4 Gy radiation. The data suggest that propofol has a radio-protective effect against IR-induced hematopoietic system damage through reducing cellular ROS in HSCs and HPCs partly through the Nrf2 pathway. |
format | Online Article Text |
id | pubmed-9075036 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | The Royal Society of Chemistry |
record_format | MEDLINE/PubMed |
spelling | pubmed-90750362022-05-09 The protective effect of propofol on ionizing radiation-induced hematopoietic system damage in mice Han, Xiaoliang Sun, Fengtao Zhang, Ying Wang, Jinyan Liu, Qingguo Gao, Ping Zhang, Shubo RSC Adv Chemistry The hematopoietic system is highly sensitive to ionizing radiation (IR), and IR can cause injury to hematopoietic stem cells (HSCs); the main reason for this may be elevated reactive oxygen species (ROS) levels. Propofol is an anesthetic drug commonly used in clinical practice. The chemical structure of propofol is similar to that of vitamin E, and propofol has an antioxidant capacity. Therefore, in this work the effect of using propofol to protect against IR-induced hematopoietic system injury is evaluated. The data suggested that when the irradiated mice were treated with 20 mg kg(−1) of propofol, the survival rate of lethally irradiated mice increased significantly, furthermore, the radiation-induced decrease of white blood cells (WBCs), red blood cells (RBCs), hemoglobin (HGC) and platelets (PLT) in peripheral blood is improved significantly. In addition, propofol could also increase the irradiated HSC and hematopoietic progenitor cell (HPC) frequencies, improving the self-renewal and differentiation abilities of HSCs and HPCs in irradiated mice. Next the ROS levels in HSCs and HPCs were measured, and the results showed that propofol could effectively decrease the ROS levels in these cells. The underlying ROS-scavenging mechanisms are further explored, and the results show that the Nrf2 pathway plays an important role in propofol's radiation protective effects, however, propofol can also increase the proliferation of the Nrf2 inhibitor-treated Lineage(−) cells after exposure to 4 Gy radiation. The data suggest that propofol has a radio-protective effect against IR-induced hematopoietic system damage through reducing cellular ROS in HSCs and HPCs partly through the Nrf2 pathway. The Royal Society of Chemistry 2019-11-08 /pmc/articles/PMC9075036/ /pubmed/35540614 http://dx.doi.org/10.1039/c9ra07262d Text en This journal is © The Royal Society of Chemistry https://creativecommons.org/licenses/by-nc/3.0/ |
spellingShingle | Chemistry Han, Xiaoliang Sun, Fengtao Zhang, Ying Wang, Jinyan Liu, Qingguo Gao, Ping Zhang, Shubo The protective effect of propofol on ionizing radiation-induced hematopoietic system damage in mice |
title | The protective effect of propofol on ionizing radiation-induced hematopoietic system damage in mice |
title_full | The protective effect of propofol on ionizing radiation-induced hematopoietic system damage in mice |
title_fullStr | The protective effect of propofol on ionizing radiation-induced hematopoietic system damage in mice |
title_full_unstemmed | The protective effect of propofol on ionizing radiation-induced hematopoietic system damage in mice |
title_short | The protective effect of propofol on ionizing radiation-induced hematopoietic system damage in mice |
title_sort | protective effect of propofol on ionizing radiation-induced hematopoietic system damage in mice |
topic | Chemistry |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9075036/ https://www.ncbi.nlm.nih.gov/pubmed/35540614 http://dx.doi.org/10.1039/c9ra07262d |
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