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Protective effect of Danhong injection on cerebral ischemia-reperfusion injury in rats.

AbstractETHNOPHARMACOLOGICAL RELEVANCE:
Danhong injection (DH), a Chinese medical product, is used extensively for the treatment of cerebrovascular diseases such as acutely cerebral infarction in clinic.
AIM OF THE STUDY:
To explore the protective effect and the relevant mechanisms of DH on cerebral ischemia-reperfusion (I/R) injury.
MATERIALS AND 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.
CONCLUSION:
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.
AuthorsYu He, Haitong Wan, Yueguang Du, Xiaodong Bie, Tao Zhao, Wei Fu, Panke Xing
JournalJournal of ethnopharmacology (J Ethnopharmacol) Vol. 144 Issue 2 Pg. 387-94 (Nov 21 2012) ISSN: 1872-7573 [Electronic] Ireland
PMID23010366 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2012 Elsevier Ireland Ltd. All rights reserved.
Chemical References
  • Bax protein, rat
  • Drugs, Chinese Herbal
  • Neuroprotective Agents
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein
  • danhong
  • Malondialdehyde
  • Superoxide Dismutase
Topics
  • Animals
  • Brain (drug effects, metabolism)
  • Drugs, Chinese Herbal (therapeutic use)
  • Injections, Intravenous
  • Male
  • Malondialdehyde (metabolism)
  • Neuroprotective Agents (therapeutic use)
  • Phytotherapy
  • Proto-Oncogene Proteins c-bcl-2 (metabolism)
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury (drug therapy, metabolism)
  • Superoxide Dismutase (metabolism)
  • bcl-2-Associated X Protein (metabolism)

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