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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
Author(s) -
Leung Mason C.P.,
Lo Samuel C.L.,
Siu Flora K.W.,
So K.F.
Publication year - 2002
Publication title -
lasers in surgery and medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.888
H-Index - 112
eISSN - 1096-9101
pISSN - 0196-8092
DOI - 10.1002/lsm.10096
Subject(s) - nitric oxide synthase , nitric oxide , ischemia , neuroprotection , medicine , endocrinology , cerebrum , transforming growth factor , irradiation , transforming growth factor beta , anesthesia , chemistry , central nervous system , physics , nuclear physics
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 < 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‐β1 ( P < 0.001). Conclusions Low energy laser could suppress the activity of NOS and up‐regulate the expression of TGF‐β1 after stroke in rats. Lasers Surg. Med. 31:283–288, 2002. © 2002 Wiley‐Liss, Inc.