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首页> 外文期刊>Japanese Journal of Pharmacology >Antinociceptive mechanism of Gosha-jinki-gan in streptozotocin-induced diabetic animals: role of nitric oxide in the periphery.
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Antinociceptive mechanism of Gosha-jinki-gan in streptozotocin-induced diabetic animals: role of nitric oxide in the periphery.

机译:Gosha-jinki-gan在链脲佐菌素诱导的糖尿病动物中的镇痛作用:一氧化氮在周围的作用。

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摘要

Using streptozotocin-induced diabetic mice and rats, we evaluated the antinociceptive mechanism of Gosha-jinki-gan. The antinociceptive effect of Gosha-jinki-gan (0.3 g/kg, p.o.) in diabetic mice, as determined by the tail-pressure test, was inhibited by N(G)-nitro-L-arginine methyl ester (L-NAME; 2, 5 mg/kg, i.p.). When L-NAME (10 microg) or methylene blue (500 microg) was topically administered to the intraplantar area of the hind paw, the region used for the paw-pressure test, the antinociceptive activity of Gosha-jinki-gan (0.3 g/kg, p.o.) in diabetic rats was decreased. These results suggested that the antinociceptive effect of Gosha-jinki-gan partly resulted from the peripheral action of increasingly produced nitric oxide.
机译:使用链脲佐菌素诱导的糖尿病小鼠和大鼠,我们评估了Gosha-Jinki-gan的抗伤害感受机制。 N(G)-硝基-L-精氨酸甲酯(L-NAME; N-G)抑制了Gosha-jinki-gan(0.3 g / kg,po)在糖尿病小鼠中的镇痛作用(通过尾压测试确定)。 2、5 mg / kg,ip)。将L-NAME(10微克)或亚甲蓝(500微克)局部施用于后爪的足底区域(用于爪压测试的区域),Gosha-Jinki-gan(0.3 g /公斤,po)在糖尿病大鼠中降低。这些结果表明,Gosha-Jinki-gan的抗伤害感受作用部分归因于一氧化氮产生量的增加。

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