title: Preconditioning of H2S inhalation protects against cerebral ischemia/reperfusion injury by induction of HSP70 through PI3K/Akt/Nrf2 pathway.
abstract: 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.
authors.affiliation: Department of Neurology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, China.
authors.forename: Kangxiang
authors.initials: K
authors.lastname: Ji
authors.affiliation: Department of Neurosurgery, Yangpu Hospital, Tongji University School of Medicine, Shanghai 200090, China.
authors.forename: Long
authors.initials: L
authors.lastname: Xue
authors.affiliation: Department of Neurology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, China.
authors.forename: Jiwei
authors.initials: J
authors.lastname: Cheng
authors.affiliation: Department of Neurology, Putuo Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai 200062, China. Electronic address: YuBai_Neurology@126.com.
authors.forename: Yu
authors.initials: Y
authors.lastname: Bai
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000280:Administration, Inhalation; D000818:Animals; D020520:Brain Infarction / Q000209:etiology / Q000517:prevention & control; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D004195:Disease Models, Animal; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism*; D006862:Hydrogen Sulfide / Q000008:administration & dosage / Q000494:pharmacology*; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018782:Maze Learning / Q000502:physiology / Q000528:radiation effects; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D051267:NF-E2-Related Factor 2 / Q000172:deficiency* / Q000235:genetics; D009460:Neurologic Examination; D051058:Oncogene Protein v-akt / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism; D015427:Reperfusion Injury / Q000378:metabolism / Q000517:prevention & control*; D015398:Signal Transduction / Q000187:drug effects*; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D000080242:8-Hydroxy-2'-Deoxyguanosine; D003849:Deoxyguanosine; D004791:Enzyme Inhibitors; D018840:HSP70 Heat-Shock Proteins; D006862:Hydrogen Sulfide; D015850:Interleukin-6; D008315:Malondialdehyde; D051267:NF-E2-Related Factor 2; D051058:Oncogene Protein v-akt; D019869:Phosphatidylinositol 3-Kinases; D014409:Tumor Necrosis Factor-alpha; C495636:Nfe2l2 protein, mouse
keywords: Akt; H(2)S; HSP70; Ischemia-reperfusion; Nrf2; PI3K