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慢性酒精摄入导致颊黏膜内皮素-1和一氧化氮合酶的改变。

Alterations in buccal mucosal endothelin-1 and nitric oxide synthase with chronic alcohol ingestion.

作者信息

Slomiany B L, Piotrowski J, Slomiany A

机构信息

Research Center, University of Medicine and Dentistry of New Jersey, Newark 07103-2400, USA.

出版信息

Biochem Mol Biol Int. 1998 Jul;45(4):681-8. doi: 10.1080/15216549800203082.

DOI:10.1080/15216549800203082
PMID:9713690
Abstract

Endothelin-1 (ET-1) and nitric oxide are emerging key mediators in the maintenance of mucosal homeostasis, but little is known about these substances in soft oral tissue with alcohol abuse. Hence, we examined the expression of ET-1 and activity of the constitutive nitric oxide synthase (NOS) in buccal mucosa of rats subjected to chronic ethanol diet. The immunometric assays revealed the buccal mucosal level of ET-1 in the controls at 40.2 pg/mg protein and showed a 4.1-fold increase with alcohol diet to 166.2 pg/mg protein. The NOS assays established that comparing to the controls, the alcohol diet group exhibited a 57% decrease in buccal mucosal NOS activity. Moreover, the expression of ET-1 showed an inverse correlation (r = -0.75) with the extent of the induced changes in NOS. The results suggest that an increase in vasoconstrictive ET-1 levels combined with a loss of compensatory action by the constitutive NOS may be responsible for the weakening of oral mucosal defenses in alcoholics.

摘要

内皮素 -1(ET -1)和一氧化氮是维持黏膜内环境稳定的关键介质,但对于滥用酒精的口腔软组织中这些物质的了解甚少。因此,我们检测了慢性乙醇饮食大鼠颊黏膜中ET -1的表达和组成型一氧化氮合酶(NOS)的活性。免疫测定显示,对照组颊黏膜中ET -1水平为40.2 pg/mg蛋白质,而酒精饮食组则增加了4.1倍,达到166.2 pg/mg蛋白质。NOS检测表明,与对照组相比,酒精饮食组颊黏膜NOS活性降低了57%。此外,ET -1的表达与NOS诱导变化程度呈负相关(r = -0.75)。结果表明,血管收缩性ET -1水平升高,同时组成型NOS的代偿作用丧失,可能是导致酗酒者口腔黏膜防御功能减弱的原因。

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