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CLC number: R743.3; R977.1

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Received: 2005-08-21

Revision Accepted: 2005-11-10

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Journal of Zhejiang University SCIENCE B 2006 Vol.7 No.2 P.142~147

10.1631/jzus.2006.B0142


Inhibition of mitochondria responsible for the anti-apoptotic effects of melatonin during ischemia-reperfusion


Author(s):  Han Yi-xiang, Zhang Sheng-hui, Wang Xi-ming, Wu Jian-bo

Affiliation(s):  Institute of Medical Science, the First Affiliated Hospital, Wenzhou Medical College, Wenzhou 325000, China; more

Corresponding email(s):   yxhan2001@163.com

Key Words:  Cerebellar granule cell, Ischemia-reperfusion, Cytochrome c, Melatonin


Han Yi-xiang, Zhang Sheng-hui, Wang Xi-ming, Wu Jian-bo. Inhibition of mitochondria responsible for the anti-apoptotic effects of melatonin during ischemia-reperfusion[J]. Journal of Zhejiang University Science B, 2006, 7(2): 142~147.

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author="Han Yi-xiang, Zhang Sheng-hui, Wang Xi-ming, Wu Jian-bo",
journal="Journal of Zhejiang University Science B",
volume="7",
number="2",
pages="142~147",
year="2006",
publisher="Zhejiang University Press & Springer",
doi="10.1631/jzus.2006.B0142"
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%0 Journal Article
%T Inhibition of mitochondria responsible for the anti-apoptotic effects of melatonin during ischemia-reperfusion
%A Han Yi-xiang
%A Zhang Sheng-hui
%A Wang Xi-ming
%A Wu Jian-bo
%J Journal of Zhejiang University SCIENCE B
%V 7
%N 2
%P 142~147
%@ 1673-1581
%D 2006
%I Zhejiang University Press & Springer
%DOI 10.1631/jzus.2006.B0142

TY - JOUR
T1 - Inhibition of mitochondria responsible for the anti-apoptotic effects of melatonin during ischemia-reperfusion
A1 - Han Yi-xiang
A1 - Zhang Sheng-hui
A1 - Wang Xi-ming
A1 - Wu Jian-bo
J0 - Journal of Zhejiang University Science B
VL - 7
IS - 2
SP - 142
EP - 147
%@ 1673-1581
Y1 - 2006
PB - Zhejiang University Press & Springer
ER -
DOI - 10.1631/jzus.2006.B0142


Abstract: 
Objective: To investigate a possible mechanism responsible for anti-apoptotic effects of melatonin and provide theoretical evidences for clinical therapy. Methods: ischemia-reperfusion mediated neuronal cell injury model was constructed in cerebellar granule neurons (CGNs) by deprivation of glucose, serum and oxygen in media. After ischemia, melatonin was added to the test groups to reach differential concentration during reperfusion. DNA fragmentation, mitochondrial transmembrane potential, mitochondrial cytochrome c release and caspase-3 activity were observed after subjecting cerebellar granule neurons to oxygen-glucose deprivation (OGD). Results: The results showed that OGD induced typical cell apoptosis change, DNA ladder and apoptosis-related alterations in mitochondrial functions including depression of mitochondrial transmembrane potential (its maximal protection ratio was 73.26%) and release of cytochrome c (its maximal inhibition ratio was 42.52%) and the subsequent activation of caspase-3 (its maximal protection ratio was 59.32%) in cytoplasm. melatonin reduced DNA damage and inhibited release of mitochondrial cytochrome c and activation of caspase-3. melatonin can strongly prevent the OGD-induced loss of the mitochondria membrane potential. Conclusion: Our findings suggested that the direct inhibition of mitochondrial pathway might essentially contribute to its anti-apoptotic effects in neuronal ischemia-reperfusion.

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