The neuroprotective effect of eupatilin against ischemia/reperfusion-induced delayed neuronal damage in mice
- Authors
- Cai, Mudan; Phan, Phuong-Thuy T.; Hong, Jin Gyu; Kim, Dong Hyun; Kim, Jong Min; Park, Se Jin; Liu, Xiaotong; Han, Jeong Eun; Park, Haeil; Choi, Ji Woong; Ryu, Jong Hoon
- Issue Date
- 15-Aug-2012
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- Eupatilin; Transient global ischemia; Neuroprotection; Akt signaling
- Citation
- EUROPEAN JOURNAL OF PHARMACOLOGY, v.689, no.1-3, pp.104 - 110
- Journal Title
- EUROPEAN JOURNAL OF PHARMACOLOGY
- Volume
- 689
- Number
- 1-3
- Start Page
- 104
- End Page
- 110
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/16231
- DOI
- 10.1016/j.ejphar.2012.05.042
- ISSN
- 0014-2999
- Abstract
- Eupatilin, a pharmacologically active flavone derived from the Artemisia plant species, has been reported to have anti-oxidant, anti-inflammatory, anti-allergic, and anti-tumor activities. In the present study, we investigated whether eupatilin exhibits neuroprotective activities against ischemia/reperfusion-induced delayed neuronal injury in mice. Transient global cerebral ischemia was induced in mice by bilateral common carotid artery occlusion (BCCAO) for 15 min followed by reperfusion for 4 days. Eupatilin (1, 3, or 10 mg/kg, p.o.) was administered immediately after the reperfusion. Histochemical studies showed that eupatilin (10 mg/kg) increased the number of viable cells detected by Nissl staining and decreased the number of degenerating neuronal cells detected by Fluoro-Jade B staining in the hippocampal CA1 region. Western blotting indicated that eupatilin further increased the level of Akt phosphorylation at 8 h after BCCAO. Furthermore, wortmannin, a phosphatidylinositol 3-kinase inhibitor, attenuated the eupatilin-induced increase of Akt phosphorylation. In addition, wortmannin completely reversed the eupatilin-induced neuroprotective effects observed at 4 days after reperfusion. These findings suggest that eupatilin is a promising therapeutic agent against global cerebral ischemia-induced neuronal damage and that its neuroprotective effects may be mediated in part by increased Akt phosphorylation. (C) 2012 Elsevier B.V. All rights reserved.
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