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标题：Protective effects of (6R)-5,6,7,8-tetrahydro-L-biopterin on local ischemia/reperfusion-induced suppression of reactive hyperemia in rat gingiva
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作者：Yusaku Tanaka ; Toshizo Toyama ; Satoko Wada-Takahashi 等
期刊名称：Journal of Clinical Biochemistry and Nutrition
印刷版ISSN：0912-0009
电子版ISSN：1880-5086
出版年度：2016
卷号：58
期号：1
页码：69-75
DOI：10.3164/jcbn.15-69
出版社：The Society for Free Radical Research Japan
摘要：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 N ^ω-nitro- l -arginine-methyl-ester ( l -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- l -biopterin (BH₄), and sepiapterin. The luminescent intensity of superoxide anion (O₂^•−)-induced 2-methyl-6-(4-methoxyphenyl)-3,7-dihydroimidazo-[1,2-a] pyrazine-3-one (MCLA) was markedly decreased by SOD and BH₄, but only slightly by sepiapterin. BH₄ significantly decreased O₂^•− 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 BH₄ by O₂^•−, played a partial role in this inhibition.
关键词：nitric oxide synthases;reperfusion;BH4;gingiva;reactive hyperemia