胃泌素对大鼠胃的保护作用涉及传入神经元、降钙素基因相关肽和一氧化氮。

Protection by gastrin in the rat stomach involves afferent neurons, calcitonin gene-related peptide, and nitric oxide.

作者信息

Stroff T, Plate S, Respondek M, Müller K M, Peskar B M

机构信息

Department of Experimental Clinical Medicine, Ruhr-University of Bochum, Germany.

出版信息

Gastroenterology. 1995 Jul;109(1):89-97. doi: 10.1016/0016-5085(95)90272-4.

DOI:10.1016/0016-5085(95)90272-4

PMID:7541004

Abstract

BACKGROUND & AIMS: Certain gut peptides exert gastroprotective effects. However, the underlying mechanism is not fully understood. This study examines the contribution of afferent neurons, calcitonin gene-related peptide, and nitric oxide to the protection conferred by gastrin 17 in the rat stomach.

METHODS

Gastroprotection by gastrin 17 against ethanol-induced gross and histological damage was studied after capsaicin-induced defunctionalization of afferent neurons, pretreatment with the calcitonin gene-related peptide receptor antagonist human calcitonin gene-related peptide8-37, anti-calcitonin gene-related peptide antibodies, and the NO synthase inhibitor NG-nitro-L-arginine.

RESULTS

Gastrin 17 (1-25 pmol/kg) dose-dependently prevented mucosal damage caused by ethanol. Protection was inhibited by functional ablation of afferent neurons or pretreatment with human calcitonin gene-related peptide8-37 (50% inhibitory dose, 86 pmol.kg-1.min-1), anticalcitonin gene-related peptide antibodies, or NG-nitro-L-arginine (50% inhibitory dose, 1 mg/kg). L-Arginine but not D-arginine reversed the effect of NG-nitro-L-arginine. Effects on gross damage were paralleled by histology. Protective doses of gastrin 17 increased gastric mucosal blood flow and, in addition, elevated plasma gastrin concentrations to the same extent as intragastric peptone perfusion.

CONCLUSIONS

Gastrin 17 has potent gastroprotective activity that involves afferent neurons, calcitonin gene-related peptide, and NO.

摘要

背景与目的

某些肠道肽具有胃保护作用。然而，其潜在机制尚未完全明确。本研究探讨传入神经元、降钙素基因相关肽和一氧化氮在胃泌素17对大鼠胃保护作用中的贡献。

方法

在辣椒素使传入神经元失功能后，给予降钙素基因相关肽受体拮抗剂人降钙素基因相关肽8 - 37、抗降钙素基因相关肽抗体以及一氧化氮合酶抑制剂NG - 硝基 - L - 精氨酸预处理，研究胃泌素17对乙醇诱导的大体和组织学损伤的胃保护作用。

结果

胃泌素17（1 - 25 pmol/kg）剂量依赖性地预防乙醇引起的黏膜损伤。传入神经元功能缺失或用人降钙素基因相关肽8 - 37（半数抑制剂量，86 pmol·kg⁻¹·min⁻¹）、抗降钙素基因相关肽抗体或NG - 硝基 - L - 精氨酸（半数抑制剂量，1 mg/kg）预处理可抑制这种保护作用。L - 精氨酸而非D - 精氨酸可逆转NG - 硝基 - L - 精氨酸的作用。大体损伤的影响与组织学结果一致。胃泌素17的保护剂量可增加胃黏膜血流量，此外，还可使血浆胃泌素浓度升高至与胃内灌注蛋白胨相同的程度。