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L-NAME prevents GM1 ganglioside-induced vasodilation in the rat brain.

机译:L-NAME可防止GM1神经节苷脂诱导的大鼠脑血管舒张。

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摘要

Monosialoganglioside (GM1) is a glycosphingolipid present in most cell membranes that displays antioxidant and neuroprotective properties. It has been recently described that GM1 induces vasodilation. However, the mechanisms underlying GM1-induced vasodilation were not evaluated to date. Therefore, in this study we investigated whether the nonspecific NOS inhibitor l-NAME prevents GM1-induced vasodilation in rats. The systemic injection of GM1 (50mg/kg, i.p.) increased the outer diameter of pial vessels by 50% in anesthetized animals at 30min, and this effect was fully prevented by the administration of the nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME, 60mg/kg, i.p. 15min before GM1 injection). A 30min exposure of cerebral cortex slices to GM1 (100microM) increased the content of nitrite plus nitrate (NOx) by 50%. Addition of l-NAME (100microM) to the incubation medium fully prevented GM1-induced NOx increase. Conversely, a 60min exposure of slices to GM1 (100microM) decreased NOx content, revealing a biphasic effect of GM1. Our results suggest that NO plays an important role in the vasodilation induced by GM1.
机译:单唾液酸神经节苷脂(GM1)是存在于大多数细胞膜中的糖鞘脂,具有抗氧化和神经保护特性。最近已经描述了GM1诱导血管舒张。但是,迄今为止尚未评估GM1诱导的血管舒张的潜在机制。因此,在这项研究中,我们调查了非特异性NOS抑制剂1-NAME是否能阻止GM1诱导的大鼠血管舒张。全身注射GM1(50mg / kg,ip)在30分钟时可使麻醉动物的乳头血管外径增加50%,并且通过使用一氧化氮合酶抑制剂N(G)-硝基- l-精氨酸甲酯(l-NAME,60mg / kg,在GM1注射前腹腔注射15分钟)。大脑皮层切片暴露于GM1(100microM)30分钟后,亚硝酸盐和硝酸盐(NOx)的含量增加了50%。将l-NAME(100microM)添加到孵育培养基中完全阻止了GM1诱导的NOx的增加。相反,将切片暴露在GM1(100microM)中60分钟会降低NOx含量,从而揭示GM1的双相效应。我们的结果表明,NO在GM1诱导的血管舒张中起重要作用。

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