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Research ArticleOriginal Article
Open Access

Melatonin attenuates hippocampal neuron apoptosis and oxidative stress during chronic intermittent hypoxia via up-regulating B-cell lymphoma-2 and down-regulating B-cell lymphoma-2-associated X protein

Xiaoqin Tan, Xueling Guo and Huiguo Liu
Saudi Medical Journal July 2013, 34 (7) 701-708;
Xiaoqin Tan
Wuhan Brain Hospital, General Hospital of the Yangtze River Shipping, Wuhan, China
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Xueling Guo
Wuhan Brain Hospital, General Hospital of the Yangtze River Shipping, Wuhan, China
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Huiguo Liu
Wuhan Brain Hospital, General Hospital of the Yangtze River Shipping, Wuhan, China
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Abstract

OBJECTIVE: To investigate the neuroprotective effect of melatonin against chronic intermittent hypoxia (CIH), the major pathophysiologic features of obstructive sleep apnea syndrome.

METHODS: This study was conducted between January 2011 and September 2012 in Tongji Hospital, Huazhong University of Science and Technology, Wuhan, China. Thirty 8-week Wistar rats were randomly divided into 3 groups (10 each): a control group, a vehicle-treated CIH group; and a melatonin-treated (10 mg/kg) CIH group. Rats were exposed to either intermittent hypoxia (IH) (oxygen concentration changing periodically from 21.78+/-0.65 to 6.57+/-0.57%), or air-air cycling at a rate of 30 cycles/hour, 8 hour/day for 4 weeks.

RESULTS: The CIH exposure led to a significant decrease in superoxide dismutase (SOD) activity and anti-apoptotic protein B-cell lymphoma-2 (BCL-2) expression in the hippocampus of CIH group rats compared with that of the control group and melatonin-treated CIH group. In contrast, hippocampal neuronal apoptosis increased significantly in parallel to an augment in 3,4-methylenedioxyamphetamine (MDA) content and pro-apoptotic protein Bcl-2-associated X protein (BAX) expression in CIH group than the other 2 groups. Melatonin administration abrogated the increase in MDA activity, as well as BAX expression, and restored SOD activity and BCL-2 expression to nearly their normal levels.

CONCLUSION: These results indicate melatonin can inhibit hippocampal neuron apoptosis following CIH by scavenging reactive oxygen species, up-regulating anti-apoptotic protein BCL-2 and down-regulating pro-apoptotic protein BAX, and thus, alleviate CIH-induced oxidative stress injury and produce neuroprotection effects.

  • Copyright: © Saudi Medical Journal

This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial License (CC BY-NC), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Saudi Medical Journal: 34 (7)
Saudi Medical Journal
Vol. 34, Issue 7
1 Jul 2013
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Melatonin attenuates hippocampal neuron apoptosis and oxidative stress during chronic intermittent hypoxia via up-regulating B-cell lymphoma-2 and down-regulating B-cell lymphoma-2-associated X protein
Xiaoqin Tan, Xueling Guo, Huiguo Liu
Saudi Medical Journal Jul 2013, 34 (7) 701-708;

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Melatonin attenuates hippocampal neuron apoptosis and oxidative stress during chronic intermittent hypoxia via up-regulating B-cell lymphoma-2 and down-regulating B-cell lymphoma-2-associated X protein
Xiaoqin Tan, Xueling Guo, Huiguo Liu
Saudi Medical Journal Jul 2013, 34 (7) 701-708;
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© 2025 Saudi Medical Journal Saudi Medical Journal is copyright under the Berne Convention and the International Copyright Convention.  Saudi Medical Journal is an Open Access journal and articles published are distributed under the terms of the Creative Commons Attribution-NonCommercial License (CC BY-NC). Readers may copy, distribute, and display the work for non-commercial purposes with the proper citation of the original work. Electronic ISSN 1658-3175. Print ISSN 0379-5284.

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