RESUMEN
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.
Asunto(s)
Apoptosis/efectos de la radiación , Ataque Isquémico Transitorio/radioterapia , Terapia por Luz de Baja Intensidad , Animales , Caspasa 3/metabolismo , Ataque Isquémico Transitorio/metabolismo , Ataque Isquémico Transitorio/patología , Masculino , Fosforilación/efectos de la radiación , Proyectos Piloto , Proteínas Proto-Oncogénicas c-akt/metabolismo , Proteínas Proto-Oncogénicas c-bcl-2/metabolismo , Ratas , Ratas Sprague-Dawley , Proteína Letal Asociada a bcl/metabolismoAsunto(s)
Hemorragia Intracraneal Traumática/etiología , Ataque Isquémico Transitorio/etiología , Plasmacitoma/diagnóstico , Neoplasias Craneales/diagnóstico , Anciano , Biopsia , Examen de la Médula Ósea , Angiografía Cerebral , Femenino , Humanos , Hemorragia Intracraneal Traumática/radioterapia , Ataque Isquémico Transitorio/radioterapia , Angiografía por Resonancia Magnética , Plasmacitoma/complicaciones , Plasmacitoma/radioterapia , Neoplasias Craneales/complicaciones , Neoplasias Craneales/diagnóstico por imagen , Tomografía Computarizada por Rayos X , Resultado del TratamientoRESUMEN
BACKGROUND AND OBJECTIVES: Nitric oxide (NO) has been shown to be neurotoxic while transforming growth factor-beta 1 (TGF-beta1) is neuroprotective in the stroke model. The present study investigates the effects of low energy laser on nitric oxide synthase (NOS) and TGF-beta1 activities after cerebral ischemia and reperfusion injury. STUDY DESIGN/MATERIALS AND METHODS: Cerebral ischemia was induced for 1 hour in male adult Sprague-Dawley (S.D.) rats with unilateral occlusion of middle cerebral artery (MCAO). Low energy laser irradiation was then applied to the cerebrum at different durations (1, 5, or 10 minutes). The activity of NOS and the expression of TGF-beta1 were evaluated in groups with different durations of laser irradiation. RESULTS: After ischemia, the activity of NOS was gradually increased from day 3, became significantly higher from day 4 to 6 (P < 0.001), but returned to the normal level after day 7. The activity and expression of the three isoforms of NOS were significantly suppressed (P < 0.001) to different extents after laser irradiation. In addition, laser irradiation was shown to trigger the expression of TGF-beta1 (P < 0.001). CONCLUSIONS: Low energy laser could suppress the activity of NOS and up-regulate the expression of TGF-beta1 after stroke in rats.