title: Fasudil hydrochloride could promote axonal growth through inhibiting the activity of ROCK.
abstract: OBJECTIVE
  This study aims to investigate the neuroprotective effect of Rho kinase inhibitor fasudil hydrochloride in ischemia/reperfusion injury N2a neuron.
  
  
  METHODS
  In vitro, N2a cells induced by ischemia and ischemia-reperfusion were treated with fasudil hydrochloride, cell damage was analyzed by MTT. On the other hand, the cytoskeleton of N2a cells was scanned through immunofluorescence techniques by Confocal Laser Microscopy which stained with FITC-phalloidin for F-actin visualization.
  
  
  RESULTS
  The activation of ROCK-II increased significantly in the damaged local during the following phase of ischemia/reperfusion injury. Ischemia induced a striking reorganization of actin cytoskeleton with a weakening of fluorescent intensity of the peripheral filament actin bands and formation of the long and thick stress fibers, but pretreatment of Fasudil hydrochloride could reversed the changes of ultra-structure on the cellular surface. MTT assay showed that Fasudil hydrochloride could prolong the survival time of the N2a cells after mimic ischemia-reperfusion for 24 h.
  
  
  CONCLUSIONS
  The activation of ROCK-II has an exceptional hoist after ischemia/reperfusion injury, it is likely to induce the collapse of the growth cone through MLC-P. Fasudil hydrochloride could promote axonal growth on inhibitory of ROCK activity.
authors.affiliation: Department of Orthopedics, Zhongnan Hospital of Wuhan University Wuhan 430071, Hubei, P. R. China.
authors.forename: Wei-Dong
authors.initials: WD
authors.lastname: Xiao
authors.affiliation: Department of Orthopedics, Zhongnan Hospital of Wuhan University Wuhan 430071, Hubei, P. R. China.
authors.forename: Ai-Xi
authors.initials: AX
authors.lastname: Yu
authors.affiliation: Department of Orthopedics, Zhongnan Hospital of Wuhan University Wuhan 430071, Hubei, P. R. China.
authors.forename: Dan-Li
authors.initials: DL
authors.lastname: Liu
mesh_terms: D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine / Q000031:analogs & derivatives* / Q000494:pharmacology; D000199:Actins / Q000378:metabolism; D000818:Animals; D001369:Axons / Q000187:drug effects* / Q000201:enzymology / Q000648:ultrastructure; D045744:Cell Line, Tumor; D002470:Cell Survival / Q000187:drug effects; D003599:Cytoskeleton / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D004789:Enzyme Activation; D051379:Mice; D018994:Myosin Light Chains / Q000378:metabolism; D018696:Neuroprotective Agents / Q000494:pharmacology*; D010766:Phosphorylation; D047428:Protein Kinase Inhibitors / Q000494:pharmacology*; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000201:enzymology / Q000473:pathology; D015398:Signal Transduction / Q000187:drug effects; D013997:Time Factors; D054460:rho-Associated Kinases / Q000037:antagonists & inhibitors* / Q000378:metabolism
chemical_list: D000199:Actins; D018994:Myosin Light Chains; D018696:Neuroprotective Agents; D047428:Protein Kinase Inhibitors; D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; C515854:Rock1 protein, mouse; C515855:Rock2 protein, mouse; D054460:rho-Associated Kinases; C049347:fasudil
keywords: Fasudil hydrochloride; ROCK; ischemia/reperfusion injury; neuroprotection