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首页> 外文期刊>Life sciences >Nicotine stimulates pepsinogen secretion from guinea pig gastric chief cells in monolayer culture.
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Nicotine stimulates pepsinogen secretion from guinea pig gastric chief cells in monolayer culture.

机译：尼古丁在单层培养中刺激豚鼠胃主要细胞的胃蛋白酶原分泌。

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摘要

We evaluated the effects of nicotine on pepsinogen secretion in vitro, using a monolayer culture system of guinea pig gastric chief cells. Pepsinogen secretion was increased by above 5 mM nicotine in a dose-dependent manner, as was the elevation of intracellular free calcium concentration ([Ca2+]i). The pepsinogen secretion stimulated by 10 mM nicotine was inhibited by above 1 mM d-tubocurarine, a nicotinic receptor antagonist, but not by same concentrations of scopolamine hydrobromide monohydrate or pirenzepine, a muscarinic receptor antagonist. The elevation of [Ca2+]i induced by 5 mM nicotine was also reduced by 10 mM d-tubocurarine, but not by 10 mM pirenzepine. A calmodulin inhibitor, N-(6-aminohexyl)-5-chloro-1-naphthalene-sulfonamide (W-7), at the concentration of 10(-6) M and a myosin light-chain kinase inhibitor, 1-(5-chloronaphthalene-1-sulfonyl)-1H-hexahydro-1,4-diazepine (ML-9), at concentrations above 10(-7) M also significantly blocked 10 mM nicotine-induced pepsinogen secretion. These finding indicate that nicotine directly stimulates pepsinogen secretion probably via nicotinic receptors on the gastric chief cells, and that the Ca(2+)-mediated messenger system, including calmodulin and myosin light-chain kinase, is involved in this event.
机译：我们使用豚鼠胃主要细胞的单层培养系统评估了尼古丁对体外胃蛋白酶原分泌的影响。胃蛋白酶原分泌增加了5 mM以上的尼古丁，呈剂量依赖性，细胞内游离钙浓度（[Ca2 +] i）升高。 10 mM尼古丁刺激的胃蛋白酶原分泌被烟碱样受体拮抗剂1 mM d-微管尿素抑制，但同浓度的东pol碱氢溴酸盐一水合物或哌仑西平（毒蕈碱受体拮抗剂）抑制。 5 mM尼古丁诱导的[Ca2 +] i升高也降低了10 mM d-微管尿素，但没有降低10 mM哌仑西平。浓度为10（-6）M的钙调蛋白抑制剂N-（6-氨基己基）-5-氯-1-萘磺酰胺（W-7）和肌球蛋白轻链激酶抑制剂1-（5 -氯萘-1-磺酰基）-1H-六氢-1,4-二氮杂（（ML-9）在浓度高于10（-7）M时也显着阻断10 mM烟碱诱导的胃蛋白酶原分泌。这些发现表明，尼古丁可能直接通过胃主要细胞上的烟碱样受体刺激胃蛋白酶原分泌，而Ca（2+）介导的信使系统，包括钙调蛋白和肌球蛋白轻链激酶，参与了这一事件。

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