title: Carvedilol protects bone marrow stem cells against hydrogen peroxide-induced cell death via PI3K-AKT pathway.
abstract: Carvedilol, a nonselective β-adrenergic receptor blocker, has been reported to exert potent anti-oxidative activities. In the present study, we aimed to investigate the effects of carvedilol against hydrogen peroxide (H2O2)-induced bone marrow-derived mesenchymal stem cells (BMSCs) death, which imitate the microenvironment surrounding transplanted cells in the injured spinal cord in vitro. Carvedilol significantly reduced H2O2-induced reactive oxygen species production, apoptosis and subsequent cell death. LY294002, the PI3K inhibitor, blocked the protective effects and up-regulation of Akt phosphorylation of carvedilol. Together, our results showed that carvedilol protects H2O2-induced BMSCs cell death partly through PI3K-Akt pathway, suggesting carvedilol could be used in combination with BMSCs for the treatment of spinal cord injury by improving the cell survival and oxidative stress microenvironments.
authors.affiliation: Guangdong Provincial Acadamy of Chinese Medical Sciences, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510120, China; Laboratory Affiliated to National Key Discipline of Orthopaedic and Traumatology of Chinese Medicine, Guangzhou University of Chinese Medicine,Guangzhou 510405, China.
authors.forename: Meihui
authors.initials: M
authors.lastname: Chen
authors.affiliation: Guangdong Provincial Acadamy of Chinese Medical Sciences, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510120, China.
authors.forename: Shudong
authors.initials: S
authors.lastname: Chen
authors.affiliation: Guangdong Provincial Acadamy of Chinese Medical Sciences, Guangdong Provincial Hospital of Chinese Medicine, Guangzhou 510120, China; Laboratory Affiliated to National Key Discipline of Orthopaedic and Traumatology of Chinese Medicine, Guangzhou University of Chinese Medicine,Guangzhou 510405, China. Electronic address: lindingkun@126.com.
authors.forename: Dingkun
authors.initials: D
authors.lastname: Lin
mesh_terms: D000818:Animals; D001854:Bone Marrow Cells / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism; D002227:Carbazoles / Q000494:pharmacology*; D000077261:Carvedilol; D016923:Cell Death / Q000187:drug effects; D048430:Cell Shape / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D019610:Cytoprotection / Q000187:drug effects*; D005434:Flow Cytometry; D006861:Hydrogen Peroxide / Q000633:toxicity*; D008297:Male; D010084:Oxidation-Reduction / Q000187:drug effects; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D011412:Propanolamines / Q000494:pharmacology*; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism*; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D013234:Stem Cells / Q000166:cytology* / Q000187:drug effects / Q000378:metabolism
chemical_list: D002227:Carbazoles; D011412:Propanolamines; D017382:Reactive Oxygen Species; D000077261:Carvedilol; D006861:Hydrogen Peroxide; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt
keywords: Bone marrow stem cells; Carvedilol; Oxidative stress; PI3K-Akt pathway; Spinal cord injury