Preconditioning of H2S inhalation protects against cerebral ischemia/reperfusion injury by induction of HSP70 through PI3K/Akt/Nrf2 pathway
•H2S preconditioning exhibited significant neuroprotection against cerebral I/R.•The protective effect of H2S preconditioning involves heat shock protein 70 (HSP70).•HSP70 protects mice against cerebral I/R through PI3K/Akt/Nrf2 pathway. It is of great importance to protect the brain against cerebra...
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| Veröffentlicht in: | Brain research bulletin 2016-03, Vol.121, p.68-74 |
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| description | •H2S preconditioning exhibited significant neuroprotection against cerebral I/R.•The protective effect of H2S preconditioning involves heat shock protein 70 (HSP70).•HSP70 protects mice against cerebral I/R through PI3K/Akt/Nrf2 pathway.
It is of great importance to protect the brain against cerebral ischemia and reperfusion (I/R) injury, which leads to excitotoxicity, redox imbalance, inflammation and apoptosis; however, there is currently no effective treatment. The present study aimed to investigate the effect of H2S preconditioning on cerebral I/R injury and its underlying mechanism. The results demonstrated that H2S preconditioning significantly prevented the development of neurological function abnormality, inflammation and oxidative injury in mice as well as cognitive impairment caused by cerebral I/R. H2S preconditioning also suppressed the apoptosis caused by cerebral I/R. Moreover, the protective effect of H2S preconditioning was found to involve heat shock protein 70 (HSP70), in which the PI3K/Akt/Nrf2 pathway was involved. The data showed that H2S preconditioning could protect mice against cerebral I/R injury by the induction of HSP70 and the PI3K/Akt/Nrf2 pathway. |
| doi_str_mv | 10.1016/j.brainresbull.2015.12.007 |
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It is of great importance to protect the brain against cerebral ischemia and reperfusion (I/R) injury, which leads to excitotoxicity, redox imbalance, inflammation and apoptosis; however, there is currently no effective treatment. The present study aimed to investigate the effect of H2S preconditioning on cerebral I/R injury and its underlying mechanism. The results demonstrated that H2S preconditioning significantly prevented the development of neurological function abnormality, inflammation and oxidative injury in mice as well as cognitive impairment caused by cerebral I/R. H2S preconditioning also suppressed the apoptosis caused by cerebral I/R. Moreover, the protective effect of H2S preconditioning was found to involve heat shock protein 70 (HSP70), in which the PI3K/Akt/Nrf2 pathway was involved. The data showed that H2S preconditioning could protect mice against cerebral I/R injury by the induction of HSP70 and the PI3K/Akt/Nrf2 pathway.</description><identifier>ISSN: 0361-9230</identifier><identifier>EISSN: 1873-2747</identifier><identifier>DOI: 10.1016/j.brainresbull.2015.12.007</identifier><identifier>PMID: 26772627</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Administration, Inhalation ; Akt ; Animals ; Brain Infarction - etiology ; Brain Infarction - prevention & control ; Deoxyguanosine - analogs & derivatives ; Deoxyguanosine - metabolism ; Disease Models, Animal ; Enzyme Inhibitors - pharmacology ; H2S ; HSP70 ; HSP70 Heat-Shock Proteins - metabolism ; Hydrogen Sulfide - administration & dosage ; Hydrogen Sulfide - pharmacology ; Interleukin-6 - metabolism ; Ischemia-reperfusion ; Male ; Malondialdehyde - metabolism ; Maze Learning - physiology ; Maze Learning - radiation effects ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neurologic Examination ; NF-E2-Related Factor 2 - deficiency ; NF-E2-Related Factor 2 - genetics ; Nrf2 ; Oncogene Protein v-akt - metabolism ; Phosphatidylinositol 3-Kinases - metabolism ; PI3K ; Reperfusion Injury - metabolism ; Reperfusion Injury - prevention & control ; Signal Transduction - drug effects ; Tumor Necrosis Factor-alpha - metabolism</subject><ispartof>Brain research bulletin, 2016-03, Vol.121, p.68-74</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0361923015300794$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26772627$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ji, Kangxiang</creatorcontrib><creatorcontrib>Xue, Long</creatorcontrib><creatorcontrib>Cheng, Jiwei</creatorcontrib><creatorcontrib>Bai, Yu</creatorcontrib><title>Preconditioning of H2S inhalation protects against cerebral ischemia/reperfusion injury by induction of HSP70 through PI3K/Akt/Nrf2 pathway</title><title>Brain research bulletin</title><addtitle>Brain Res Bull</addtitle><description>•H2S preconditioning exhibited significant neuroprotection against cerebral I/R.•The protective effect of H2S preconditioning involves heat shock protein 70 (HSP70).•HSP70 protects mice against cerebral I/R through PI3K/Akt/Nrf2 pathway.
It is of great importance to protect the brain against cerebral ischemia and reperfusion (I/R) injury, which leads to excitotoxicity, redox imbalance, inflammation and apoptosis; however, there is currently no effective treatment. The present study aimed to investigate the effect of H2S preconditioning on cerebral I/R injury and its underlying mechanism. The results demonstrated that H2S preconditioning significantly prevented the development of neurological function abnormality, inflammation and oxidative injury in mice as well as cognitive impairment caused by cerebral I/R. H2S preconditioning also suppressed the apoptosis caused by cerebral I/R. Moreover, the protective effect of H2S preconditioning was found to involve heat shock protein 70 (HSP70), in which the PI3K/Akt/Nrf2 pathway was involved. The data showed that H2S preconditioning could protect mice against cerebral I/R injury by the induction of HSP70 and the PI3K/Akt/Nrf2 pathway.</description><subject>Administration, Inhalation</subject><subject>Akt</subject><subject>Animals</subject><subject>Brain Infarction - etiology</subject><subject>Brain Infarction - prevention & control</subject><subject>Deoxyguanosine - analogs & derivatives</subject><subject>Deoxyguanosine - metabolism</subject><subject>Disease Models, Animal</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>H2S</subject><subject>HSP70</subject><subject>HSP70 Heat-Shock Proteins - metabolism</subject><subject>Hydrogen Sulfide - administration & dosage</subject><subject>Hydrogen Sulfide - pharmacology</subject><subject>Interleukin-6 - metabolism</subject><subject>Ischemia-reperfusion</subject><subject>Male</subject><subject>Malondialdehyde - metabolism</subject><subject>Maze Learning - physiology</subject><subject>Maze Learning - radiation effects</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Neurologic Examination</subject><subject>NF-E2-Related Factor 2 - deficiency</subject><subject>NF-E2-Related Factor 2 - genetics</subject><subject>Nrf2</subject><subject>Oncogene Protein v-akt - metabolism</subject><subject>Phosphatidylinositol 3-Kinases - metabolism</subject><subject>PI3K</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Signal Transduction - drug effects</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><issn>0361-9230</issn><issn>1873-2747</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkc1u1DAURi0EokPhFZDFik0y_ndmWZXSVlQwUru3HOd64iGTDLYDmmfgpevQIrFkZcs6-u79fBD6QElNCVXrfd1GG8YIqZ2HoWaEypqymhD9Aq1oo3nFtNAv0YpwRasN4-QMvUlpTwhRjVSv0RlTWjPF9Ar93kZw09iFHKYxjDs8eXzD7nEYezvY5REf45TB5YTtrkxNGTuIUDYYcEiuh0Ow6whHiH5OCx7G_RxPuD2VWze7PxFL6P1WE5z7OM27Hm9v-Zf1xfe8_ho9w0eb-1_29Ba98nZI8O75PEcPn68eLm-qu2_Xt5cXdxVwInPVCiKk96Rrm9KokdQ7AG6VVxzANx0n1DeWcOmF7aho-cbDRkDHhXJCK36OPj7FlmI_ZkjZHEoRGAY7wjQnQ3UjmRRCbP4D1VQzoSUt6PtndG4P0JljDAcbT-bvVxfg0xMApdrPANEkF2B00IWiIJtuCoYSsxg2e_OvYbMYNpSZYpg_AsGlnjA</recordid><startdate>201603</startdate><enddate>201603</enddate><creator>Ji, Kangxiang</creator><creator>Xue, Long</creator><creator>Cheng, Jiwei</creator><creator>Bai, Yu</creator><general>Elsevier Inc</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>201603</creationdate><title>Preconditioning of H2S inhalation protects against cerebral ischemia/reperfusion injury by induction of HSP70 through PI3K/Akt/Nrf2 pathway</title><author>Ji, Kangxiang ; Xue, Long ; Cheng, Jiwei ; Bai, Yu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-e305t-b4045ff0db8000851fcee3a6f63eef8d301f8a035f4ad14b39fe94ed346c4763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Administration, Inhalation</topic><topic>Akt</topic><topic>Animals</topic><topic>Brain Infarction - etiology</topic><topic>Brain Infarction - prevention & control</topic><topic>Deoxyguanosine - analogs & derivatives</topic><topic>Deoxyguanosine - metabolism</topic><topic>Disease Models, Animal</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>H2S</topic><topic>HSP70</topic><topic>HSP70 Heat-Shock Proteins - metabolism</topic><topic>Hydrogen Sulfide - administration & dosage</topic><topic>Hydrogen Sulfide - pharmacology</topic><topic>Interleukin-6 - metabolism</topic><topic>Ischemia-reperfusion</topic><topic>Male</topic><topic>Malondialdehyde - metabolism</topic><topic>Maze Learning - physiology</topic><topic>Maze Learning - radiation effects</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Neurologic Examination</topic><topic>NF-E2-Related Factor 2 - deficiency</topic><topic>NF-E2-Related Factor 2 - genetics</topic><topic>Nrf2</topic><topic>Oncogene Protein v-akt - metabolism</topic><topic>Phosphatidylinositol 3-Kinases - metabolism</topic><topic>PI3K</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Signal Transduction - drug effects</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ji, Kangxiang</creatorcontrib><creatorcontrib>Xue, Long</creatorcontrib><creatorcontrib>Cheng, Jiwei</creatorcontrib><creatorcontrib>Bai, Yu</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Brain research bulletin</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ji, Kangxiang</au><au>Xue, Long</au><au>Cheng, Jiwei</au><au>Bai, Yu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Preconditioning of H2S inhalation protects against cerebral ischemia/reperfusion injury by induction of HSP70 through PI3K/Akt/Nrf2 pathway</atitle><jtitle>Brain research bulletin</jtitle><addtitle>Brain Res Bull</addtitle><date>2016-03</date><risdate>2016</risdate><volume>121</volume><spage>68</spage><epage>74</epage><pages>68-74</pages><issn>0361-9230</issn><eissn>1873-2747</eissn><abstract>•H2S preconditioning exhibited significant neuroprotection against cerebral I/R.•The protective effect of H2S preconditioning involves heat shock protein 70 (HSP70).•HSP70 protects mice against cerebral I/R through PI3K/Akt/Nrf2 pathway.
It is of great importance to protect the brain against cerebral ischemia and reperfusion (I/R) injury, which leads to excitotoxicity, redox imbalance, inflammation and apoptosis; however, there is currently no effective treatment. The present study aimed to investigate the effect of H2S preconditioning on cerebral I/R injury and its underlying mechanism. The results demonstrated that H2S preconditioning significantly prevented the development of neurological function abnormality, inflammation and oxidative injury in mice as well as cognitive impairment caused by cerebral I/R. H2S preconditioning also suppressed the apoptosis caused by cerebral I/R. Moreover, the protective effect of H2S preconditioning was found to involve heat shock protein 70 (HSP70), in which the PI3K/Akt/Nrf2 pathway was involved. The data showed that H2S preconditioning could protect mice against cerebral I/R injury by the induction of HSP70 and the PI3K/Akt/Nrf2 pathway.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26772627</pmid><doi>10.1016/j.brainresbull.2015.12.007</doi><tpages>7</tpages></addata></record> |
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| subjects | Administration, Inhalation Akt Animals Brain Infarction - etiology Brain Infarction - prevention & control Deoxyguanosine - analogs & derivatives Deoxyguanosine - metabolism Disease Models, Animal Enzyme Inhibitors - pharmacology H2S HSP70 HSP70 Heat-Shock Proteins - metabolism Hydrogen Sulfide - administration & dosage Hydrogen Sulfide - pharmacology Interleukin-6 - metabolism Ischemia-reperfusion Male Malondialdehyde - metabolism Maze Learning - physiology Maze Learning - radiation effects Mice Mice, Inbred C57BL Mice, Transgenic Neurologic Examination NF-E2-Related Factor 2 - deficiency NF-E2-Related Factor 2 - genetics Nrf2 Oncogene Protein v-akt - metabolism Phosphatidylinositol 3-Kinases - metabolism PI3K Reperfusion Injury - metabolism Reperfusion Injury - prevention & control Signal Transduction - drug effects Tumor Necrosis Factor-alpha - metabolism |
| title | Preconditioning of H2S inhalation protects against cerebral ischemia/reperfusion injury by induction of HSP70 through PI3K/Akt/Nrf2 pathway |
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