Protective effects of (6R)-5,6,7,8-tetrahydro-L-biopterin on local ischemia/reperfusion-induced suppression of reactive hyperemia in rat gingiva
Access this Article
Search this Article
We herein investigated the regulatory mechanism in the circulation responsible for rat gingival reactive hyperemia (RH) associated with ischemia/reperfusion (I/R). RH was analyzed using a laser Doppler flowmeter. RH and I/R were elicited by gingival compression and release with a laser Doppler probe. RH increased in a time-dependent manner when the duration of compression was between 30 s and 20 min. This increase was significantly suppressed by <i>N</i><sup>ω</sup>-nitro-<span style="font-variant: small-caps;">l</span>-arginine-methyl-ester (<span style="font-variant: small-caps;">l</span>-NAME), 7-nitroindazole (7-NI), and 2,4-diamino-6-hydroxypyrimidine (DAHP). However, RH was markedly inhibited following 60 min of compression. This inhibition was significantly decreased by treatments with superoxide dismutase (SOD), (6R)-5,6,7,8-tetrahydro-<span style="font-variant: small-caps;">l</span>-biopterin (BH<sub>4</sub>), and sepiapterin. The luminescent intensity of superoxide anion (O<sub>2</sub><sup>•−</sup>)-induced 2-methyl-6-(4-methoxyphenyl)-3,7-dihydroimidazo-[1,2-a] pyrazine-3-one (MCLA) was markedly decreased by SOD and BH<sub>4</sub>, but only slightly by sepiapterin. BH<sub>4</sub> significantly decreased O<sub>2</sub><sup>•−</sup> scavenging activity in a time-dependent manner. These results suggested that nitric oxide (NO) secreted by the nitrergic nerve played a role in regulating local circulation in rat gingiva. This NO-related regulation of local circulation was temporarily inhibited in the gingiva by the I/R treatment. The decrease observed in the production of NO, which was caused by suppression of NO synthase (NOS) activity subsequent to depletion of the NOS co-factor BH<sub>4</sub> by O<sub>2</sub><sup>•−</sup>, played a partial role in this inhibition.
- Journal of Clinical Biochemistry and Nutrition
Journal of Clinical Biochemistry and Nutrition 58(1), 69-75, 2016
SOCIETY FOR FREE RADICAL RESEARCH JAPAN