期刊
EXPERIMENTAL AND TOXICOLOGIC PATHOLOGY
卷 61, 期 2, 页码 137-143出版社
ELSEVIER GMBH, URBAN & FISCHER VERLAG
DOI: 10.1016/j.etp.2008.06.004
关键词
Apoptosis; Hypoxia; Reoxygenation; JNK; p38
资金
- National Natural Scientific Foundation of China [30472010]
- Doctorial Subject-specific Scientific Research Foundation [20030558092]
- Natural Scientific Foundation of Guangdong Province [039191]
As a model of the reperfusion injury found in stroke, we treated cerebellar granule neurons (CGNs) with hypoxia followed by reoxygenation. Hypoxia for 3 h followed by 24 h reoxygenation (H/R) induced a typical apoptosis of CGNs. CGNs exposed to H/R responded by activating JNK, increasing the expression of p38 and ultimately caused CGNs dying. Furthermore, apoptosis of CGNs induced by H/R was inhibited by pre-treatment with SB203580 or SP600125, and the inhibitory effect of SB203580 was greater than that of SP600125. Additionally, we also found that H/R temporally activated Akt and inactivated glycogen synthesis kinase-3 beta (GSK-3 beta), two proteins the functions of which were important in cell survival and energy metabolism. These findings demonstrated that H/R-induced apoptosis in CGNs by enhancing JNK and p38 activity, which contributed at least in part to H/R-induced apoptosis of CGNs. (C) 2008 Elsevier GmbH. All rights reserved.
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