title: Protective effect of Danhong injection on cerebral ischemia-reperfusion injury in rats.
abstract: BACKGROUND
  Danhong injection (DH), a Chinese medical product, is used extensively for the treatment of cerebrovascular diseases such as acutely cerebral infarction in clinic.
  
  
  OBJECTIVE
  To explore the protective effect and the relevant mechanisms of DH on cerebral ischemia-reperfusion (I/R) injury.
  
  
  METHODS
  Cerebral I/R injury was induced through four-vessel occlusion (4-VO) or middle cerebral artery occlusion (MCAO). Adult male SD rats were randomly divided into six kinds of groups: normal control group, sham-operated group, I/R injury group, DH-treated groups at doses of 0.5ml/kg, 1.0ml/kg and 2.0ml/kg. The effects of DH on murine neurological deficits and cerebral infarct volume, 6-keto-prostagladin F(1α) (6-keto-PGF(1α)) level, malondialdehyde (MDA) level and superoxide dismutase (SOD) activity in brain tissue, as well as the activities of plasma tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) after I/R were evaluated. Moreover, the expressions of Bcl-2 and Bax protein were detected by immunohistochemistry.
  
  
  RESULTS
  There was no significant difference between the control group and the sham-operated group based on the measurement indicators. Compared with the vehicle-treated group, rats treated with DH showed dose dependent reductions in brain infarction size, and improvement of neurological outcome. The level of 6-keto-PGF(1α) and the activities of SOD and plasma t-PA were enhanced significantly, whereas the level of MDA and the activity of plasma PAI were declined significantly. The immunohistochemical staining results also revealed that the expression of Bcl-2 protein was up-regulated and that of Bax protein was down-regulated when exposed to DH.
  
  
  CONCLUSIONS
  DH demonstrates a strong ameliorative effect on cerebral I/R damage in rats by its anticoagulant, antithrombotic, antifibrinolytic and antioxidant activities. Furthermore, suppressing apoptosis through regulating Bcl-2 and Bax protein expressions should be another potential mechanism by which DH exerts its neuroprotective function.
authors.affiliation: College of Bioengineering, Zhejiang Chinese Medical University, 548 Binwen Road, Hangzhou, Zhejiang, China.
authors.forename: Yu
authors.initials: Y
authors.lastname: He
authors.forename: Haitong
authors.initials: H
authors.lastname: Wan
authors.forename: Yueguang
authors.initials: Y
authors.lastname: Du
authors.forename: Xiaodong
authors.initials: X
authors.lastname: Bie
authors.forename: Tao
authors.initials: T
authors.lastname: Zhao
authors.forename: Wei
authors.initials: W
authors.lastname: Fu
authors.forename: Panke
authors.initials: P
authors.lastname: Xing
mesh_terms: D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D004365:Drugs, Chinese Herbal / Q000627:therapeutic use*; D007275:Injections, Intravenous; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D008517:Phytotherapy; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: C494828:Bax protein, rat; D004365:Drugs, Chinese Herbal; D018696:Neuroprotective Agents; D019253:Proto-Oncogene Proteins c-bcl-2; D051028:bcl-2-Associated X Protein; C540581:danhong; D008315:Malondialdehyde; D013482:Superoxide Dismutase