Astaxanthin attenuates total body irradiation-induced hematopoietic system injury in mice via inhibition of oxidative stress and apoptosis
The hematopoietic system is especially sensitive to total body irradiation (TBI), and myelosuppression is one of the major effects of TBI. Astaxanthin (ATX) is a powerful natural anti-oxidant with low toxicity. In this study, the effect of ATX on hematopoietic system injury after TBI was investigate...
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| Veröffentlicht in: | Stem cell research & therapy 2017-01, Vol.8 (1), p.7-7, Article 7 |
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| creator | Xue, Xiao-Lei Han, Xiao-Dan Li, Yuan Chu, Xiao-Fei Miao, Wei-Min Zhang, Jun-Ling Fan, Sai-Jun |
| description | The hematopoietic system is especially sensitive to total body irradiation (TBI), and myelosuppression is one of the major effects of TBI. Astaxanthin (ATX) is a powerful natural anti-oxidant with low toxicity. In this study, the effect of ATX on hematopoietic system injury after TBI was investigated.
Flow cytometry was used to detect the proportion of hematopoietic progenitor cells (HPCs) and hematopoietic stem cells (HSCs), the level of intracellular reactive oxygen species (ROS), expression of cytochrome C, cell apoptosis, and NRF2-related proteins. Immunofluorescence staining was used to detect Nrf2 translocation. Western blot analysis was used to evaluate the expression of apoptotic-related proteins. Enzymatic activities assay kits were used to analyze SOD2, CAT, and GPX1 activities.
Compared with the TBI group, ATX can improve radiation-induced skewed differentiation of peripheral blood cells and accelerate hematopoietic self-renewal and regeneration. The radio-protective effect of ATX is probably attributable to the scavenging of ROS and the reduction of cell apoptosis. These changes were associated with increased activation of Nrf2 and downstream anti-oxidative proteins, and regulation of apoptotic-related proteins.
This study suggests that ATX could be used as a potent therapeutic agent to protect the hematopoietic system against TBI-induced bone marrow suppression. |
| doi_str_mv | 10.1186/s13287-016-0464-3 |
| format | Article |
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Flow cytometry was used to detect the proportion of hematopoietic progenitor cells (HPCs) and hematopoietic stem cells (HSCs), the level of intracellular reactive oxygen species (ROS), expression of cytochrome C, cell apoptosis, and NRF2-related proteins. Immunofluorescence staining was used to detect Nrf2 translocation. Western blot analysis was used to evaluate the expression of apoptotic-related proteins. Enzymatic activities assay kits were used to analyze SOD2, CAT, and GPX1 activities.
Compared with the TBI group, ATX can improve radiation-induced skewed differentiation of peripheral blood cells and accelerate hematopoietic self-renewal and regeneration. The radio-protective effect of ATX is probably attributable to the scavenging of ROS and the reduction of cell apoptosis. These changes were associated with increased activation of Nrf2 and downstream anti-oxidative proteins, and regulation of apoptotic-related proteins.
This study suggests that ATX could be used as a potent therapeutic agent to protect the hematopoietic system against TBI-induced bone marrow suppression.</description><identifier>ISSN: 1757-6512</identifier><identifier>EISSN: 1757-6512</identifier><identifier>DOI: 10.1186/s13287-016-0464-3</identifier><identifier>PMID: 28115023</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Analysis ; Animals ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - radiation effects ; Astaxanthin ; Blood Cells - cytology ; Blood Cells - drug effects ; Blood Cells - radiation effects ; Body Weight - drug effects ; Body Weight - radiation effects ; Bone Marrow Cells - cytology ; Bone Marrow Cells - radiation effects ; Cell Differentiation - drug effects ; Complications and side effects ; Control ; Dosage and administration ; Glutathione Peroxidase - metabolism ; Health aspects ; Hematopoietic stem cells ; Hematopoietic Stem Cells - cytology ; Hematopoietic Stem Cells - metabolism ; Hematopoietic System - drug effects ; Hematopoietic System - injuries ; Hematopoietic System - radiation effects ; Ionizing radiation ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria - drug effects ; Mitochondria - metabolism ; Mitochondria - radiation effects ; NF-E2-Related Factor 2 - deficiency ; NF-E2-Related Factor 2 - genetics ; NF-E2-Related Factor 2 - metabolism ; Oxidative Stress - drug effects ; Oxidative Stress - radiation effects ; Proto-Oncogene Proteins c-kit - metabolism ; Reactive Oxygen Species - metabolism ; Superoxide Dismutase - metabolism ; Whole-Body Irradiation ; Xanthophylls - pharmacology</subject><ispartof>Stem cell research & therapy, 2017-01, Vol.8 (1), p.7-7, Article 7</ispartof><rights>COPYRIGHT 2017 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2017</rights><rights>The Author(s). 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c559t-61797919377b4c18dbcaac5e5be644e86826a05f0e36de3ee6fcf437c794efc63</citedby><cites>FETCH-LOGICAL-c559t-61797919377b4c18dbcaac5e5be644e86826a05f0e36de3ee6fcf437c794efc63</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5260077/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5260077/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28115023$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Xue, Xiao-Lei</creatorcontrib><creatorcontrib>Han, Xiao-Dan</creatorcontrib><creatorcontrib>Li, Yuan</creatorcontrib><creatorcontrib>Chu, Xiao-Fei</creatorcontrib><creatorcontrib>Miao, Wei-Min</creatorcontrib><creatorcontrib>Zhang, Jun-Ling</creatorcontrib><creatorcontrib>Fan, Sai-Jun</creatorcontrib><title>Astaxanthin attenuates total body irradiation-induced hematopoietic system injury in mice via inhibition of oxidative stress and apoptosis</title><title>Stem cell research & therapy</title><addtitle>Stem Cell Res Ther</addtitle><description>The hematopoietic system is especially sensitive to total body irradiation (TBI), and myelosuppression is one of the major effects of TBI. Astaxanthin (ATX) is a powerful natural anti-oxidant with low toxicity. In this study, the effect of ATX on hematopoietic system injury after TBI was investigated.
Flow cytometry was used to detect the proportion of hematopoietic progenitor cells (HPCs) and hematopoietic stem cells (HSCs), the level of intracellular reactive oxygen species (ROS), expression of cytochrome C, cell apoptosis, and NRF2-related proteins. Immunofluorescence staining was used to detect Nrf2 translocation. Western blot analysis was used to evaluate the expression of apoptotic-related proteins. Enzymatic activities assay kits were used to analyze SOD2, CAT, and GPX1 activities.
Compared with the TBI group, ATX can improve radiation-induced skewed differentiation of peripheral blood cells and accelerate hematopoietic self-renewal and regeneration. The radio-protective effect of ATX is probably attributable to the scavenging of ROS and the reduction of cell apoptosis. These changes were associated with increased activation of Nrf2 and downstream anti-oxidative proteins, and regulation of apoptotic-related proteins.
This study suggests that ATX could be used as a potent therapeutic agent to protect the hematopoietic system against TBI-induced bone marrow suppression.</description><subject>Analysis</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - radiation effects</subject><subject>Astaxanthin</subject><subject>Blood Cells - cytology</subject><subject>Blood Cells - drug effects</subject><subject>Blood Cells - radiation effects</subject><subject>Body Weight - drug effects</subject><subject>Body Weight - radiation effects</subject><subject>Bone Marrow Cells - cytology</subject><subject>Bone Marrow Cells - radiation effects</subject><subject>Cell Differentiation - drug effects</subject><subject>Complications and side effects</subject><subject>Control</subject><subject>Dosage and administration</subject><subject>Glutathione Peroxidase - metabolism</subject><subject>Health aspects</subject><subject>Hematopoietic stem cells</subject><subject>Hematopoietic Stem Cells - cytology</subject><subject>Hematopoietic Stem Cells - metabolism</subject><subject>Hematopoietic System - drug effects</subject><subject>Hematopoietic System - injuries</subject><subject>Hematopoietic System - radiation effects</subject><subject>Ionizing radiation</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mitochondria - drug effects</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - radiation effects</subject><subject>NF-E2-Related Factor 2 - deficiency</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>NF-E2-Related Factor 2 - metabolism</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - radiation effects</subject><subject>Proto-Oncogene Proteins c-kit - metabolism</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Whole-Body Irradiation</subject><subject>Xanthophylls - 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drug effects</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - radiation effects</topic><topic>NF-E2-Related Factor 2 - deficiency</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>NF-E2-Related Factor 2 - metabolism</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - radiation effects</topic><topic>Proto-Oncogene Proteins c-kit - metabolism</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Whole-Body Irradiation</topic><topic>Xanthophylls - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xue, Xiao-Lei</creatorcontrib><creatorcontrib>Han, Xiao-Dan</creatorcontrib><creatorcontrib>Li, Yuan</creatorcontrib><creatorcontrib>Chu, Xiao-Fei</creatorcontrib><creatorcontrib>Miao, Wei-Min</creatorcontrib><creatorcontrib>Zhang, Jun-Ling</creatorcontrib><creatorcontrib>Fan, Sai-Jun</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Stem cell research & therapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xue, Xiao-Lei</au><au>Han, Xiao-Dan</au><au>Li, Yuan</au><au>Chu, Xiao-Fei</au><au>Miao, Wei-Min</au><au>Zhang, Jun-Ling</au><au>Fan, Sai-Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Astaxanthin attenuates total body irradiation-induced hematopoietic system injury in mice via inhibition of oxidative stress and apoptosis</atitle><jtitle>Stem cell research & therapy</jtitle><addtitle>Stem Cell Res Ther</addtitle><date>2017-01-23</date><risdate>2017</risdate><volume>8</volume><issue>1</issue><spage>7</spage><epage>7</epage><pages>7-7</pages><artnum>7</artnum><issn>1757-6512</issn><eissn>1757-6512</eissn><abstract>The hematopoietic system is especially sensitive to total body irradiation (TBI), and myelosuppression is one of the major effects of TBI. Astaxanthin (ATX) is a powerful natural anti-oxidant with low toxicity. In this study, the effect of ATX on hematopoietic system injury after TBI was investigated.
Flow cytometry was used to detect the proportion of hematopoietic progenitor cells (HPCs) and hematopoietic stem cells (HSCs), the level of intracellular reactive oxygen species (ROS), expression of cytochrome C, cell apoptosis, and NRF2-related proteins. Immunofluorescence staining was used to detect Nrf2 translocation. Western blot analysis was used to evaluate the expression of apoptotic-related proteins. Enzymatic activities assay kits were used to analyze SOD2, CAT, and GPX1 activities.
Compared with the TBI group, ATX can improve radiation-induced skewed differentiation of peripheral blood cells and accelerate hematopoietic self-renewal and regeneration. The radio-protective effect of ATX is probably attributable to the scavenging of ROS and the reduction of cell apoptosis. These changes were associated with increased activation of Nrf2 and downstream anti-oxidative proteins, and regulation of apoptotic-related proteins.
This study suggests that ATX could be used as a potent therapeutic agent to protect the hematopoietic system against TBI-induced bone marrow suppression.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>28115023</pmid><doi>10.1186/s13287-016-0464-3</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Analysis Animals Apoptosis Apoptosis - drug effects Apoptosis - radiation effects Astaxanthin Blood Cells - cytology Blood Cells - drug effects Blood Cells - radiation effects Body Weight - drug effects Body Weight - radiation effects Bone Marrow Cells - cytology Bone Marrow Cells - radiation effects Cell Differentiation - drug effects Complications and side effects Control Dosage and administration Glutathione Peroxidase - metabolism Health aspects Hematopoietic stem cells Hematopoietic Stem Cells - cytology Hematopoietic Stem Cells - metabolism Hematopoietic System - drug effects Hematopoietic System - injuries Hematopoietic System - radiation effects Ionizing radiation Male Mice Mice, Inbred C57BL Mice, Knockout Mitochondria - drug effects Mitochondria - metabolism Mitochondria - radiation effects NF-E2-Related Factor 2 - deficiency NF-E2-Related Factor 2 - genetics NF-E2-Related Factor 2 - metabolism Oxidative Stress - drug effects Oxidative Stress - radiation effects Proto-Oncogene Proteins c-kit - metabolism Reactive Oxygen Species - metabolism Superoxide Dismutase - metabolism Whole-Body Irradiation Xanthophylls - pharmacology |
| title | Astaxanthin attenuates total body irradiation-induced hematopoietic system injury in mice via inhibition of oxidative stress and apoptosis |
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