Please use this identifier to cite or link to this item: http://hdl.handle.net/10397/29569
Title: The effect of low-energy laser irradiation on apoptotic factors following experimentally induced transient cerebral ischemia
Authors: Yip, KK
Lo, SCL 
Leung, MCP
So, KF
Tang, CY
Poon, DMY
Keywords: Apoptosis
Caspase
Ischemia
Laser
Stroke
Issue Date: 2011
Publisher: Pergamon-Elsevier Science Ltd
Source: Neuroscience, 2011, v. 190, p. 301-306 How to cite?
Journal: Neuroscience 
Abstract: Apoptosis, or programmed cell death, resulting from cerebral ischemia may be related to decreased levels of anti-apoptotic factors, such as serine/threonine kinase (Akt), phosphorylated Akt (pAkt), pBAD, and Bcl-2, and increased levels of pro-apoptotic factors, such as BAD, caspase 9, and caspase 3 activities. In this study, we investigated the effects of low-energy laser (660 nm) irradiation (LLI) on the levels and activity of various anti- and pro-apoptotic factors following ischemia. Transient cerebral ischemia was induced in Sprague-Dawley rats by unilateral occlusion of the middle cerebral artery for 1 h, followed by reperfusion. LLI was then directed on the cerebrum for varying lengths of duration (1, 5, or 10 min at an energy density of 2.64 J/cm 2, 13.2 J/cm 2, and 24.6 J/cm 2, respectively). The expression levels of Akt, pAkt, BAD, pBAD, Bcl-2, caspase 9, and caspase 3 activities were measured 4 days after injury. The levels of Akt, pAkt, Bcl-2, and pBAD were significantly increased following laser irradiation. In addition, LLI significantly decreased caspase 9 and caspase 3 activities caused by ischemia-reperfusion. LLI may protect the brain by upregulating Akt, pAkt, pBAD, and Bcl-2 expression and downregulating caspase 9 and caspase 3 expression following transient cerebral ischemia. This modality is a promising protective therapeutic intervention after strokes or other ischemic events.
URI: http://hdl.handle.net/10397/29569
DOI: 10.1016/j.neuroscience.2011.06.022
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