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压力与胃部:促肾上腺皮质激素释放因子可能通过糖皮质激素参与在压力状态下保护胃黏膜。

Stress and the Stomach: Corticotropin-Releasing Factor May Protect the Gastric Mucosa in Stress Through Involvement of Glucocorticoids.

作者信息

Filaretova Ludmila, Bagaeva Tatiana, Morozova Olga

机构信息

Laboratory of Experimental Endocrinology, Pavlov Institute of Physiology, Russian Academy of Sciences, nab. Makarova 6, St. Petersburg, Russia, 199034,

出版信息

Cell Mol Neurobiol. 2012 Jul;32(5):829-836. doi: 10.1007/s10571-012-9800-z. Epub 2012 Feb 1.

Abstract

Stress may contribute to the development of gastric ulcer disease. The results of our previous investigations suggest that glucocorticoids released during acute stress act as gastroprotective hormones, and not as ulcerogenic agents as has been generally accepted for a long time. In this study, we investigated whether corticotropin-releasing factor (CRF) may protect the gastric mucosa against stress-induced gastric injury through involvement of glucocorticoids. Intraperitoneal administration of CRF (1.25 μg/kg, 30 min before stress) markedly increased plasma corticosterone level (at 15 and 30 min after the administration) and significantly suppressed the occurrence of gastric erosion induced by 3-h cold-restraint stress (at 10°C) in conscious rats. To test the participation of corticosterone in the gastroprotective effect of exogenous CRF, two approaches were used: pretreatment by the inhibitor of glucocorticoid synthesis, metyrapone (30 mg/kg, i.p.) and the antagonist of glucocorticoid receptors RU-38486 (20 mg/kg, i.p.). Metyrapone injected shortly before CRF administration caused a fast inhibition of CRF-induced corticosterone response and reversed the protective effect of CRF on the gastric mucosa against the stress-induced erosion. The gastroprotective effect of CRF was also attenuated by the pretreatment rats with glucocorticoid receptor antagonist RU-38486. The results suggest that exogenous CRF may protect the gastric mucosa against stress-induced gastric injury through involvement of glucocorticoids.

摘要

应激可能促使胃溃疡疾病的发生。我们之前的研究结果表明,急性应激期间释放的糖皮质激素起到胃保护激素的作用,而非如长期以来普遍认为的那样是致溃疡因子。在本研究中,我们调查了促肾上腺皮质激素释放因子(CRF)是否可能通过糖皮质激素的参与来保护胃黏膜免受应激诱导的胃损伤。腹腔注射CRF(1.25μg/kg,在应激前30分钟)显著提高了血浆皮质酮水平(在注射后15和30分钟),并显著抑制了清醒大鼠在3小时冷束缚应激(10°C)诱导的胃糜烂的发生。为了测试皮质酮在外源性CRF胃保护作用中的参与情况,采用了两种方法:用糖皮质激素合成抑制剂美替拉酮(30mg/kg,腹腔注射)和糖皮质激素受体拮抗剂RU - 38486(20mg/kg,腹腔注射)进行预处理。在CRF给药前不久注射美替拉酮导致CRF诱导的皮质酮反应快速抑制,并逆转了CRF对胃黏膜免受应激诱导糜烂的保护作用。用糖皮质激素受体拮抗剂RU - 38486预处理大鼠也减弱了CRF的胃保护作用。结果表明,外源性CRF可能通过糖皮质激素的参与来保护胃黏膜免受应激诱导的胃损伤。

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