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

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  Ethnopharmacological 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.Meterals and methods: Cerebral I/R injury was induced through four-vessel occlusion (4-VO) or middle cereoral 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 0.5 ml/kg,1.0 ml/kg and 2.0 ml/kg.The effects of DH on murine neurological deficits and cerebral infarct volume,6-keto-prostagladin F1α (6-keto-PGF1α) 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-PGF1α and the activities of SOD and plasma t-PA were enhanced significantly, whereas the level of MDA and the activity of plasma PN 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 downregulated when exposed to DH.Conclusion: DH demonstrates a strong ameliorative effect on cerebral I/R damage in rats by its anticoagulant, antithro(m)botic, antifibrinolytic and antioxidant activities.Furthermore, suppressing apoptosis through regulating Bd-2 and Bax protein expressions should be another potential mechanism by which DH exerts its neuroprotective function.
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