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前列腺素E2导致乳鼠肠道大分子转运和消化酶发育过早停止。

Precocious cessation of intestinal macromolecular transport and digestive enzymes development by prostaglandin E2 in suckling rats.

作者信息

Harada E, Hashimoto Y, Syuto B

机构信息

Department of Physiology, Hokkaido University, Sapporo, Japan.

出版信息

Comp Biochem Physiol Physiol. 1994 Oct;109(2):245-53. doi: 10.1016/0300-9629(94)90127-9.

Abstract

The effect of repeated oral administration of prostaglandin analogue (dmPGE2) on intestinal macromolecular transport and digestive enzymes development were investigated in the suckling rats. By the administration of dmPGE2 for 7 days, precocious induction of maltase activity, depression of amylase activity and enhancement of trypsin activity in the pancreas occurred. Absorption of bovine IgG was dose dependently depressed by dmPGE2 treatments. The intestinal cessation was also observed in the adrenalectomized pups, but was not influenced by difluoromethyl ornithine administration. These results suggest that oral administration of PGE2 induces precocious maturation of the small intestine and exocrine pancreas and that the intestinal cessation is not directly related to ornithine decarboxylase activity in the suckling rats.

摘要

在乳鼠中研究了重复口服前列腺素类似物(dmPGE2)对肠道大分子转运和消化酶发育的影响。通过给予dmPGE2 7天,胰腺中麦芽糖酶活性早熟诱导、淀粉酶活性降低以及胰蛋白酶活性增强。dmPGE2处理剂量依赖性地抑制牛IgG的吸收。在肾上腺切除的幼崽中也观察到肠道停止,但不受二氟甲基鸟氨酸给药的影响。这些结果表明,口服PGE2可诱导小肠和外分泌胰腺早熟成熟,并且在乳鼠中肠道停止与鸟氨酸脱羧酶活性没有直接关系。

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