分子和药理依据调制激肽B(1)受体表达的内源性糖皮质激素荷尔蒙的老鼠。

文章的细节

引用

复制到剪贴板

卡布里尼哒,坎波斯MM, Tratsk KS,美利奴VF,席尔瓦JA Jr, Souza通用电气、Avellar MC, Pesquero JB,卡利斯托简森-巴顿

分子和药理依据调制激肽B(1)受体表达的内源性糖皮质激素荷尔蒙的老鼠。

Br J杂志。2001年1月,132 (2):567 - 77。

PubMed ID

11159707 (在PubMed

]

文摘

1。内源性糖皮质激素荷尔蒙的影响在老鼠B(1)受体的表达进行检测的分子和药理功能的方法。2。老鼠肾上腺切除(ADX),这个过程和7天后B的皮内注射(1)受体激动剂des-Arg (9) bk生产爪数量显著增加,而只有一个弱sham-operated动物的观察效果。增加一个类似的收缩反应由B(1)受体激动剂des-Arg (9) bk也观察到大鼠门静脉体外。3所示。化学ADX与米托坦(减少类固醇合成药物)产生本质上相同的B(1)受体的上调观察ADX老鼠。4所示。B的调制(1)受体的表达是由核糖核酸酶保护试验,评估使用信使rna从肺部和ADX老鼠的爪子。5。 Additionally, both paw oedema and contraction of portal vein mediated by B(1) agonist des-Arg(9)-BK in ADX rats, were markedly inhibited by treatment with dexamethasone, or COX-2 inhibitor meloxican, or with the NF-kappaB inhibitor PDTC. Interestingly, the same degree of inhibition was achieved when the animals were treated with a combination of submaximal doses of dexamethasone and PDTC. 6. The involvement of NF-kappaB pathway was further confirmed by mobility shift assay using nuclear extracts from lung, paw and heart of ADX rats. It was also confirmed that the treatment of ADX rats with dexamethasone, PDTC or dexamethasone plus PDTC completely inhibit NF-kappaB activation caused by absence of endogenous glucucorticoid. 7. Together, the results of the present study provide, for the first time, molecular and pharmacological evidence showing that B(1) kinin receptor expression can be regulated through endogenous glucocorticoids by a mechanism dependent on NF-kappaB pathway. Clinical significance of the present findings stem from evidence showing the importance of B(1) kinin receptors in the mediation of inflammatory and pain related responses.

beplay体育安全吗DrugBank数据引用了这篇文章

药物靶点

药物	目标	类	生物	药理作用	行动
米托坦	皮质铁氧还蛋白、线粒体	蛋白质	人类	未知的	未知的	细节