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内皮素可促进卵清蛋白诱导的大鼠肠道过敏反应。

Endothelins promote egg albumin-induced intestinal anaphylaxis in rats.

作者信息

Shigematsu T, Miura S, Hirokawa M, Hokari R, Higuchi H, Tsuzuki Y, Kimura H, Nakatsumi R C, Serizawa H, Saito H, Ishii H

机构信息

Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.

出版信息

Gastroenterology. 1998 Aug;115(2):348-56. doi: 10.1016/s0016-5085(98)70201-x.

Abstract

BACKGROUND & AIMS: The basic mechanisms of food allergies are still unknown. The aims of this study were to investigate whether endothelins (ETs) in the intestinal mucosa are involved in the pathogenesis of intestinal anaphylaxis.

METHODS

Sprague-Dawley rats were sensitized to chicken egg albumin (EA) by intraperitoneal injection. Fourteen days after sensitization, EA was administered in the jejunal segments to induce intestinal anaphylaxis. Net water outflux and histamine release into loops and serum concentrations of rat mast cell protease II (RMCP-II) were determined. ET-1 and ET-3 concentrations in the jejunal mucosa were determined, and expression of the corresponding messenger RNAs was examined by competitive polymerase chain reaction.

RESULTS

In sensitized animals, challenge with intraluminal antigen caused a significant increase in net water outflux and histamine release together with an elevation of serum RMCP-II concentrations. Mucosal concentrations of ET-1 and ET-3 and expression of their messenger RNAs were significantly increased in sensitized animals after EA challenge. Treatment with an ETA-receptor antagonist, but not an ETB-receptor antagonist, attenuated the increase in net water outflux, histamine release, and serum RMCP-II concentrations in rats with EA-induced intestinal anaphylaxis.

CONCLUSIONS

Release of ETs in the intestinal mucosa increased in sensitized animals after EA challenge. ETs may play a significant role in the development of intestinal anaphylaxis via an ETA receptor.

摘要

背景与目的

食物过敏的基本机制仍不清楚。本研究的目的是调查肠黏膜中的内皮素(ETs)是否参与肠道过敏反应的发病机制。

方法

通过腹腔注射使Sprague-Dawley大鼠对鸡卵白蛋白(EA)致敏。致敏14天后,在空肠段给予EA以诱导肠道过敏反应。测定净水流出量、组胺释放到肠袢中的量以及大鼠肥大细胞蛋白酶II(RMCP-II)的血清浓度。测定空肠黏膜中ET-1和ET-3的浓度,并通过竞争性聚合酶链反应检测相应信使核糖核酸的表达。

结果

在致敏动物中,腔内抗原激发导致净水流出量和组胺释放显著增加,同时血清RMCP-II浓度升高。EA激发后,致敏动物黏膜中ET-1和ET-3的浓度及其信使核糖核酸的表达显著增加。用ETA受体拮抗剂而非ETB受体拮抗剂治疗可减轻EA诱导的肠道过敏反应大鼠的净水流出量、组胺释放和血清RMCP-II浓度的增加。

结论

EA激发后,致敏动物肠黏膜中ETs的释放增加。ETs可能通过ETA受体在肠道过敏反应的发生中起重要作用。

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