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International Journal of Photoenergy
Volume 2014, Article ID 585934, 5 pages
http://dx.doi.org/10.1155/2014/585934
Research Article

Effect and Mechanism of 808 nm Light Pretreatment of Hypoxic Primary Neurons

1College of Medical Device and Food Engineering, University of Shanghai for Science and Technology, Shanghai 200093, China
2Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
3Key Laboratory of System Biology, Chinese Academy of Sciences, Shanghai 201210, China
4Laboratory of System Biology, Shanghai Advanced Research Institute, Chinese Academy of Sciences, Shanghai 201210, China

Received 9 January 2014; Accepted 29 January 2014; Published 11 March 2014

Academic Editor: Timon Cheng-Yi Liu

Copyright © 2014 Xin Chen et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

This study investigated the effect of low intensity 808 nm light pretreatment of hypoxic primary neurons. Cobalt chloride (CoCl2) has been used to induce hypoxic injury in primary mouse cortical neurons. Low intensity 808 nm light was from light-emitting diode (LED). Cells were randomly divided into 4 groups: normal control group, CoCl2-induced group, CoCl2-induced group with 808 nm light irradiation pretreatment, and normal group with 808 nm light irradiation pretreatment. Effect of low intensity 808 nm light on neuronal morphology has been observed by microscope. MTT colorimetric assay has been used to detect the effect of low intensity 808 nm light on neuronal activity. Adenosine triphosphate (ATP) concentration and cytochrome C oxidase (COX) activity has been detected to study the effect of low intensity 808 nm light on neuronal mitochondria function. The results indicated that low intensity 808 nm light pretreatment alone did not affect cell viability, COX activity, and ATP content of neurons and low intensity 808 nm light pretreatment promoted the cell viability, COX activity, and ATP content of neurons with CoCl2 exposure; however, low intensity 808 nm light pretreatment did not completely recover COX activity and cellular ATP content of primary neurons with CoCl2 exposure to the level of the normal neurons.