Treatment of experimentally induced transient cerebral ischemia with low energy laser inhibits nitric oxide synthase activity and up-regulates the expression of transforming growth factor-beta 1

Background and Objectives Nitric oxide (NO) has been shown to be neurotoxic while transforming growth factor‐beta 1 (TGF‐β1) is neuroprotective in the stroke model. The present study investigates the effects of low energy laser on nitric oxide synthase (NOS) and TGF‐β1 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‐β1 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