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牛磺胆酸盐诱导的胃黏膜损伤中内源性前列腺素和血栓素的生成

Generation of endogenous prostaglandins and thromboxanes in taurocholate-induced gastric mucosal lesions.

作者信息

Konturek S J, Brzozowski T, Radecki T, Dobrzańska M

出版信息

Scand J Gastroenterol Suppl. 1984;92:91-6.

PMID:6377475
Abstract

This study demonstrates that the suppression of thromboxane biosynthesis by OKY-1581, a selective inhibitor of thromboxane biosynthesis, prevents dose-dependently taurocholate-induced gastric mucosal necrosis and enhances the cytoprotective effect of low dose of taurocholate against mucosal necrosis by large dose of this agent. In all animals treated with OKY-1581, a decrease in mucosal generation of thromboxane was accompanied by an increased production of PGs probably due to availability of greater amounts of a common substrate in a cyclooxygenase pathway. This study provides direct evidence that gastric mucosa generates thromboxanes which may be involved in the pathogenesis of taurocholate-induced gastric mucosal lesions.

摘要

本研究表明,血栓素生物合成的选择性抑制剂OKY-1581对血栓素生物合成的抑制作用可剂量依赖性地预防牛磺胆酸盐诱导的胃黏膜坏死,并增强低剂量牛磺胆酸盐对大剂量该药物所致黏膜坏死的细胞保护作用。在用OKY-1581治疗的所有动物中,血栓素的黏膜生成减少,同时PGs生成增加,这可能是由于环氧化酶途径中更多共同底物的可用性所致。本研究提供了直接证据,表明胃黏膜会生成血栓素,其可能参与牛磺胆酸盐诱导的胃黏膜损伤的发病机制。

相似文献

1
Generation of endogenous prostaglandins and thromboxanes in taurocholate-induced gastric mucosal lesions.牛磺胆酸盐诱导的胃黏膜损伤中内源性前列腺素和血栓素的生成
Scand J Gastroenterol Suppl. 1984;92:91-6.
2
Role of prostaglandin and thromboxane biosynthesis in gastric necrosis produced by taurocholate and ethanol.前列腺素和血栓素生物合成在牛磺胆酸盐和乙醇所致胃坏死中的作用
Dig Dis Sci. 1983 Feb;28(2):154-60. doi: 10.1007/BF01315145.
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Sucralfate protection against gastrointestinal damage: possible role of prostanoids.硫糖铝对胃肠道损伤的保护作用:前列腺素的可能作用。
Isr J Med Sci. 1986 Nov;22(11):801-6.
4
Gastric mucosal prostaglandin generation in rats with stress ulcer.应激性溃疡大鼠胃黏膜前列腺素的生成
Adv Prostaglandin Thromboxane Leukot Res. 1983;12:383-7.
5
Gastric mucosal protection with selective inhibition of thromboxane synthesis.通过选择性抑制血栓素合成实现胃黏膜保护。
Gut. 1987 May;28(5):541-4. doi: 10.1136/gut.28.5.541.
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Role of prostaglandins in alkaline secretion from the gastroduodenal mucosa exposed to acid and taurocholate.
Scand J Gastroenterol Suppl. 1984;92:69-74.
7
Endogenous biosynthesis of prostaglandin I2 and thromboxane A2 by isolated rat dental pulp.大鼠离体牙髓中前列腺素I2和血栓素A2的内源性生物合成
Biochem Pharmacol. 1983 Oct 1;32(19):2983-5. doi: 10.1016/0006-2952(83)90408-2.
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Gastric cytoprotection by pirenzepine. Role of endogenous prostaglandins.哌仑西平对胃的细胞保护作用。内源性前列腺素的作用。
Scand J Gastroenterol Suppl. 1982;72:255-9.
9
[The prostaglandin and thromboxane system of the gastric mucosa as a target for protective and ulcerogenic drugs].[作为保护性和致溃疡药物作用靶点的胃黏膜前列腺素和血栓素系统]
Wien Klin Wochenschr. 1984 Feb 17;96(4):133-8.
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Prostaglandins in peptic ulcer disease: effect of nonsteroidal anti-inflammatory compounds (NOSAC).前列腺素在消化性溃疡疾病中的作用:非甾体类抗炎化合物(NOSAC)的影响。
Scand J Gastroenterol Suppl. 1984;92:250-4.

引用本文的文献

1
Prostanoids and oxygen free radicals in early stages of experimental acute pancreatitis.
Dig Dis Sci. 1994 Jul;39(7):1537-43. doi: 10.1007/BF02088061.
2
Effects of 16, 16-dimethyl prostaglandin E2 on lysosomal membrane stability in rat stomach.16,16-二甲基前列腺素E2对大鼠胃溶酶体膜稳定性的影响
J Gastroenterol. 1994 Dec;29(6):703-9. doi: 10.1007/BF02349274.
3
Protection by nitecapone against sodium taurocholate-induced damage to cultured gastric cells.
Dig Dis Sci. 1993 Apr;38(4):701-7. doi: 10.1007/BF01316803.
4
Cytoprotective effect of acetaminophen against taurocholate-induced damage to rat gastric monolayer cultures.对乙酰氨基酚对牛磺胆酸盐诱导的大鼠胃单层培养损伤的细胞保护作用。
Dig Dis Sci. 1988 Aug;33(8):938-44. doi: 10.1007/BF01535988.
5
Somatostatin stimulates prostaglandin production by rat gastric epithelial cells in vitro, but is not cytoprotective.生长抑素在体外刺激大鼠胃上皮细胞产生前列腺素,但没有细胞保护作用。
Dig Dis Sci. 1988 Nov;33(11):1435-40. doi: 10.1007/BF01536999.
6
Cysteamine protects gastric epithelial cell monolayers against drug induced damage: evidence for direct cellular protection by sulphydryl compounds.半胱胺可保护胃上皮细胞单层免受药物诱导的损伤:巯基化合物直接细胞保护作用的证据。
Gut. 1992 Jan;33(1):30-8. doi: 10.1136/gut.33.1.30.