The effect of low-energy laser irradiation on apoptotic factors following experimentally induced transient cerebral ischemia

K. K. Yip, Chun Lap Samuel Lo, M. C P Leung, K. F. So, Chak Yin Tang, D. M Y Poon

Research output: Journal article publicationJournal articleAcademic researchpeer-review

26 Citations (Scopus)


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/cm2, 13.2 J/cm2, and 24.6 J/cm2, 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.
Original languageEnglish
Pages (from-to)301-306
Number of pages6
Publication statusPublished - 5 Sep 2011


  • Apoptosis
  • Caspase
  • Ischemia
  • Laser
  • Stroke

ASJC Scopus subject areas

  • Neuroscience(all)

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