期刊
JOURNAL OF ETHNOPHARMACOLOGY
卷 144, 期 2, 页码 387-394出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2012.09.025
关键词
Danhong injection; Neuroprotection; Ischemia-reperfusion; Apoptosis; Antioxidant
资金
- Natural Science Foundation of China [30973933, 81173647, 81102734]
- Zhejiang Provincial Natural Science Foundation of China [Z2101201]
- Zhejiang Province Key Science and Technology Innovation Team [2012R10044-06]
- Zhejiang Provincial Program for the Cultivation of High-level Innovative Health Talents
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. 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 0.5 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 F-1 alpha (6-keto-PGF(1 alpha)) 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 Box 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(1 alpha) 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. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
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