title: Prolonged Fasting Improves Endothelial Progenitor Cell-Mediated Ischemic Angiogenesis in Mice.
abstract: OBJECTIVE
  Prolonged fasting (PF) was shown to be of great potency to promote optimal health and reduce the risk of many chronic diseases. This study sought to determine the effect of PF on the endothelial progenitor cell (EPC)-mediated angiogenesis in the ischemic brain and cerebral ischemic injury in mice.
  
  
  METHODS
  Mice were subjected to PF or periodic PF after cerebral ischemia, and histological analysis and behavioral tests were performed. Mouse EPCs were isolated and examined, and the effects of EPC transplantation on cerebral ischemic injury were investigated in mice.
  
  
  RESULTS
  It was found that PF significantly increased the EPC functions and angiogenesis in the ischemic brain, and attenuated the cerebral ischemic injury in mice that was previously subjected to cerebral ischemia. Periodic PF might reduce cortical atrophy and improve long-term neurobehavioral outcomes after cerebral ischemia in mice. The eNOS and MnSOD expression and intracellular NO level were increased, and TSP-2 expression and intracellular O2- level were reduced in EPCs from PF-treated mice compared to control. In addition, transplanted EPCs might home into ischemic brain, and the EPCs from PF-treated mice had a stronger ability to promote angiogenesis in ischemic brain and reduce cerebral ischemic injury compared to the EPCs from control mice. The EPC-conditioned media from PF-treated mice exerted a stronger effect on cerebral ischemic injury reduction compared to that from control mice.
  
  
  CONCLUSIONS
  Prolonged fasting promoted EPC-mediated ischemic angiogenesis and improved long-term stroke outcomes in mice. It is implied that prolonged fasting might potentially be an option to treat ischemic vascular diseases.
authors.affiliation: Department of Identification of Traditional Chinese Medicine, The Second Military Medical University, Shanghai, China.
authors.forename: Bao
authors.initials: B
authors.lastname: Xin
authors.forename: Chun-Long
authors.initials: CL
authors.lastname: Liu
authors.forename: Hong
authors.initials: H
authors.lastname: Yang
authors.forename: Cheng
authors.initials: C
authors.lastname: Peng
authors.forename: Xiao-Hui
authors.initials: XH
authors.lastname: Dong
authors.forename: Chuan
authors.initials: C
authors.lastname: Zhang
authors.forename: Alex F
authors.initials: AF
authors.lastname: Chen
authors.forename: He-Hui
authors.initials: HH
authors.lastname: Xie
mesh_terms: D000818:Animals; D001284:Atrophy; D001522:Behavior, Animal; D002545:Brain Ischemia / Q000473:pathology* / Q000503:physiopathology*; D002540:Cerebral Cortex / Q000098:blood supply / Q000187:drug effects / Q000473:pathology; D017077:Culture Media, Conditioned / Q000494:pharmacology; D066026:Endothelial Progenitor Cells / Q000187:drug effects / Q000473:pathology*; D005215:Fasting; D008297:Male; D008810:Mice, Inbred C57BL; D018919:Neovascularization, Physiologic / Q000187:drug effects; D009569:Nitric Oxide / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D017077:Culture Media, Conditioned; D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III; D013482:Superoxide Dismutase