金黄色葡萄球菌细胞壁肽聚糖对腺苷酸环化酶系统调节大鼠肌层收缩活性机制的影响。

L S Nasibyan, I B Philyppov
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引用次数: 2

摘要

本文探讨了腺苷酸环化酶调节系统各组成部分在金黄色葡萄球菌肽聚糖调节大鼠子宫肌收缩活性中的作用。用去甲肾上腺素和沙丁胺醇研究肽聚糖对肌层β-肾上腺素能受体的影响。结果表明,在这些物质的抑制下,应用肽聚糖后,肌收缩力恢复到初始水平。在cAMP水平升高的情况下,我们也观察到同样的效果。肽聚糖增强收缩的能力被8-溴基camp和罂粟碱抑制。霍乱毒素对Gi/o蛋白的刺激对肽聚糖作用没有影响,而百日咳毒素对Gi/o蛋白的阻断使其表现停止。我们得出结论,肽聚糖的调节作用是通过激活Gi/o蛋白来实现的,从而导致腺苷环化酶脱敏。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
EFFECT OF PEPTIDOGLYCANE OF STAPHYLOCOCCUS AUREUS CELL WALL ON THE MECHANISM OF REGULATION OF CONTRACTILE ACTIVITY OF RAT MYOMETRIUM BY ADENYLATE CYCLASE SYSTEM.

The revue deals with the role of each component of adenylate cyclase regulatory system in the rat myometrial contractile activity modulation by the peptidoglycane of Staphylococcus aureus. Noradrenalin and salbutamol were used to investigate peptidoglycane impact on the myometrial β-adrenergic receptors. It was shown that inhibited by these substances myometrial contractility increased to the initial level after peptidoglycane application. The same effect we observed under the cAMP level elevation by forscolin. Peptidoglycan’ s ability to strengthen contractions was inhibited by the 8-brom-cAMP and papaverine application. Stimulation of Gs-protein by the cholera toxin didn’t influence on the peptidoglycane effect while the blocking of Gi/o-protein by the pertussis toxin caused stopping it’s manifestation. We concluded that the modulating effect of peptidoglycane implemented via Gi/o-protein activation, which causes adenilatcyclase desensitization.

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