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Proliferative effect of acetylcholine on rat trachea epithelial cells is mediated by nicotinic receptors and muscarinic receptors of the M1-subtype.

机译:乙酰胆碱对大鼠气管上皮细胞的增殖作用是由M1亚型的烟碱受体和毒蕈碱受体介导的。

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摘要

Acetylcholine (ACh), synthesized in mammalian non-neuronal cells such as epithelial cells of the airways, digestive tract and skin, is involved in the regulation of basic cell functions (so-called non-neuronal cholinergic system). In the present experiments rat trachea epithelial cells have been cultured to study the proliferative effect of applied ACh by [3H]thymidine incorporation. ACh (exposure time 24 h) caused a concentration-dependent increase in cell proliferation with a doubling of the [3H]thymidine incorporation at a concentration of 0.1 microM. This effect was partly reduced by 30 microM tubocurarine and completely abolished by the additional application of 1 microM atropine. The stimulatory effect of acetylcholine, remaining in the presence of tubocurarine, was prevented by 1 microM pirenzepine (preferentially acting at M1-receptors), but neither by 1 microM AFDX 116 (preferentially acting at M2-receptors) nor by 1 microM hexahydrosiladifenidol (preferentially acting at M3-receptors). The combination of tubocurarine and pirenzepine halved the basal [3H]thymidine incorporation. In conclusion, ACh produces a proliferative effect in rat trachea epithelial cells, the effect being mediated by both nicotinic receptors and muscarinic receptors of the M1-subtype.
机译:乙酰胆碱(ACh)在哺乳动物非神经元细胞(如气道,消化道和皮肤的上皮细胞)中合成,参与基本细胞功能的调节(所谓的非神经元胆碱能系统)。在本实验中,已经培养了大鼠气管上皮细胞,以研究通过[3 H]胸苷掺入施加的乙酰胆碱的增殖作用。 ACh(暴露时间24 h)引起浓度依赖性的细胞增殖增加,在0.1 microM的浓度下[3H]胸苷掺入量增加一倍。 30 microM的微管尿素可部分减弱这种作用,而另外应用1 microM的阿托品可完全消除这种作用。 1 microM哌仑西平(优先作用于M1-受体)阻止了仍然存在于微管尿素中的乙酰胆碱的刺激作用,但1 microM AFDX 116(优先作用于M2-受体)或1 microM六氢硅二苯二酚(优选作用于M3受体)。微管尿素和哌仑西平的组合使基础[3H]胸苷的结合减半。总之,ACh在大鼠气管上皮细胞中产生增殖作用,该作用由M1亚型的烟碱样受体和毒蕈碱样受体介导。

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