title: Leonurine protects brain injury by increased activities of UCP4, SOD, CAT and Bcl-2, decreased levels of MDA and Bax, and ameliorated ultrastructure of mitochondria in experimental stroke.
abstract: BACKGROUND
  It has been proved that pre-treatment with leonurine could protect brain tissue against ischemic injury by exerting antioxidant effects and regulating mitochondrial function. Whether this protective effect applies to acute phase after cerebral ischemia, we therefore investigate the potential neuroprotective role of leonurine and the underlying mechanisms in cerebral ischemia.
  
  
  METHODS
  Focal cerebral ischemia was induced in adult male Sprague-Dawley rats by permanent middle cerebral artery occlusion (MCAO). Leonurine was administered intraperitoneally at 7.5 or 15 mg/kg/d at 2h after surgery, then once daily thereafter. Neurological deficit, brain water content, and infarct volume were measured at 24h, 72 h, and 7d after stroke. Superoxide dismutase (SOD), catalase (CAT) activities, and malondialdehyde (MDA) content were also measured by spectrophotometer to evaluate oxidative reactions, and the expression of uncoupling protein 4 (UCP4), Bcl-2, and Bax were detected by reverse transcription-polymerase chain reaction (RT-PCR), immunohistochemical staining (IHC), and western blot, while the ultrastructure of the mitochondria were observed under transmission electron microscope.
  
  
  RESULTS
  Leonurine significantly alleviated neurological deficit, decreased brain water content and infarct volume after ischemic stroke, which was accompanied by decreased levels of MDA and Bax, increased activities of SOD, CAT, UCP4, and Bcl-2, and restored ultrastructure of mitochondria.
  
  
  CONCLUSIONS
  The results showed that leonurine protected brain injury by increased activities of UCP4, SOD, CAT and Bcl-2, decreased levels of MDA and Bax, and ameliorated ultrastructure of mitochondria in experimental stroke.
authors: Department of Neurology, Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, PR China.
authors: Haichao
authors: H
authors: Liu
authors: Xiangjian
authors: X
authors: Zhang
authors: Yuanyuan
authors: Y
authors: Du
authors: Hui
authors: H
authors: Ji
authors: Shuya
authors: S
authors: Li
authors: Litao
authors: L
authors: Li
authors: Yinxue
authors: Y
authors: Xing
authors: Xiaolin
authors: X
authors: Zhang
authors: Lipeng
authors: L
authors: Dong
authors: Chaohui
authors: C
authors: Wang
authors: Kang
authors: K
authors: Zhao
authors: Ye
authors: Y
authors: Ji
authors: Xiaoyun
authors: X
authors: Cao
mesh_terms: D000818:Animals; D015153:Blotting, Western; D001930:Brain Injuries / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D005707:Gallic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D007150:Immunohistochemistry; D007473:Ion Channels / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D046529:Microscopy, Electron, Transmission; D008928:Mitochondria / Q000187:drug effects / Q000648:ultrastructure; D024101:Mitochondrial Proteins / Q000378:metabolism; D000071245:Mitochondrial Uncoupling Proteins; D018696:Neuroprotective Agents / Q000494:pharmacology*; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020133:Reverse Transcriptase Polymerase Chain Reaction; D020521:Stroke / Q000188:drug therapy* / Q000378:metabolism* / Q000473:pathology; D013482:Superoxide Dismutase / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D007473:Ion Channels; D024101:Mitochondrial Proteins; D000071245:Mitochondrial Uncoupling Proteins; D018696:Neuroprotective Agents; D019253:Proto-Oncogene Proteins c-bcl-2; C494853:Slc25a27 protein, rat; D051028:bcl-2-Associated X Protein; C013587:leonurine; D008315:Malondialdehyde; D005707:Gallic Acid; D002374:Catalase; D013482:Superoxide Dismutase