title: Neuroprotective capabilities of TSA against cerebral ischemia/reperfusion injury via PI3K/Akt signaling pathway in rats.
abstract: BACKGROUND
  Hundreds of previous studies demonstrated the cytoprotective effect of trichostatin-A (TSA), a kind of histone deacetylases inhibitors (HDACIs), against cerebral ischemia/reperfusion insult. Meanwhile, phosphatidylinositol-3 kinase/Akt (PI3K/Akt) is a well-known, important signaling pathway that mediates neuroprotection. However, it should be remains unclear whether the neuroprotective capabilities of TSA against cerebral ischemia/reperfusion is mediated by activation of the PI3K/Akt signaling pathway.
  
  
  METHODS
  Five groups rats (n = 12 each), with middle cerebral artery occlusion (MCAO) except sham group, were used to investigate the neuroprotective effect of certain concentration (0.05 mg/kg) of TSA, and whether the neuroprotective effect of TSA is associated with activation of the PI3K/Akt signaling pathway through using of wortmannin (0.25 mg/kg).
  
  
  RESULTS
  TSA significantly increased the expression of p-Akt protein, reduced infarct volume, and attenuated neurological deficit in rats with transient MCAO, wortmannin weakened such effect of TSA dramatically.
  
  
  CONCLUSIONS
  TSA could significantly decrease the neurological deficit scores and reduce the cerebral infarct volume during cerebral ischemia/reperfusion injury, which was achieved partly by activation of the PI3K/Akt signaling pathway via upgrading of p-Akt protein.
authors.affiliation: 1Department of Radiology , and.
authors.forename: Xiao-Hui
authors.initials: XH
authors.lastname: Ma
authors.forename: Qiang
authors.initials: Q
authors.lastname: Gao
authors.forename: Zhen
authors.initials: Z
authors.lastname: Jia
authors.forename: Ze-Wei
authors.initials: ZW
authors.lastname: Zhang
mesh_terms: D000704:Analysis of Variance; D000730:Androstadienes / Q000494:pharmacology; D000818:Animals; D001930:Brain Injuries / Q000209:etiology / Q000517:prevention & control; D002545:Brain Ischemia / Q000150:complications / Q000188:drug therapy*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006877:Hydroxamic Acids / Q000627:therapeutic use*; D008297:Male; D009422:Nervous System Diseases / Q000209:etiology / Q000517:prevention & control; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D051058:Oncogene Protein v-akt / Q000378:metabolism; D019869:Phosphatidylinositol 3-Kinases / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000150:complications / Q000517:prevention & control*; D015398:Signal Transduction / Q000187:drug effects*; D000077191:Wortmannin
chemical_list: D000730:Androstadienes; D004791:Enzyme Inhibitors; D006877:Hydroxamic Acids; D018696:Neuroprotective Agents; C012589:trichostatin A; D019869:Phosphatidylinositol 3-Kinases; D051058:Oncogene Protein v-akt; D000077191:Wortmannin
keywords: Akt; PI3K/Akt signal pathway; TSA; cerebral ischemia/reperfusion injury; p-Akt