title: Atorvastatin ameliorates cerebral vasospasm and early brain injury after subarachnoid hemorrhage and inhibits caspase-dependent apoptosis pathway.
abstract: BACKGROUND
  Cerebral vasospasm (CVS) and early brain injury remain major causes of morbidity and mortality after aneurysmal subarachnoid hemorrhage (SAH). Hydroxymethylglutaryl coenzyme A reductase inhibitors, also known as statins, has the neuroprotective effects and ameliorating CVS after SAH. This study was designed to explore apoptosis inhibiting effects of atorvastatin and its potential apoptotic signal pathway after SAH.
  
  
  RESULTS
  Preserving blood-brain-barrier permeability, decreasing brain edema, increasing neurological scores and ameliorating cerebral vasospasm were obtained after prophylactic use of atorvastatin. TUNEL-positive cells were reduced markedly both in basilar artery and in brain cortex by atorvastatin. Apoptosis-related proteins P53, AIF and Cytochrome C were up-regulated after SAH, while they were not affected by atorvastatin. In addition, up-regulation of caspase-3 and caspase-8 after SAH was decreased by atorvastatin treatment both in mRNA and in protein levels.
  
  
  CONCLUSIONS
  The neuroprotective effects of atorvastatin after SAH may be related to its inhibition of caspase-dependent proapoptotic pathway based on the present results.
authors.affiliation: Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin, Heilongjiang, PR China. doctorgaocheng@yahoo.com.cn
authors.forename: Gao
authors.initials: G
authors.lastname: Cheng
authors.forename: Liu
authors.initials: L
authors.lastname: Wei
authors.forename: Sun
authors.initials: S
authors.lastname: Zhi-Dan
authors.forename: Zhao
authors.initials: Z
authors.lastname: Shi-Guang
authors.forename: Liu
authors.initials: L
authors.lastname: Xiang-Zhen
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D000069059:Atorvastatin; D001812:Blood-Brain Barrier / Q000187:drug effects / Q000378:metabolism; D001921:Brain / Q000378:metabolism / Q000503:physiopathology; D001929:Brain Edema / Q000188:drug therapy; D001930:Brain Injuries / Q000188:drug therapy* / Q000209:etiology; D020169:Caspases / Q000378:metabolism; D053938:DNA Fragmentation / Q000187:drug effects; D006538:Heptanoic Acids / Q000627:therapeutic use*; D008297:Male; D018696:Neuroprotective Agents / Q000627:therapeutic use; D011758:Pyrroles / Q000627:therapeutic use*; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000503:physiopathology*; D020301:Vasospasm, Intracranial / Q000188:drug therapy* / Q000209:etiology; D014867:Water / Q000378:metabolism
chemical_list: D006538:Heptanoic Acids; D018696:Neuroprotective Agents; D011758:Pyrroles; D012333:RNA, Messenger; D014867:Water; D000069059:Atorvastatin; D020169:Caspases