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神经节苷脂对链脲佐菌素诱导糖尿病大鼠幽门括约肌神经病变的预防作用

Prevention of neuropathy in the pyloric sphincter of streptozotocin-diabetic rats by gangliosides.

作者信息

Soediono P, Belai A, Burnstock G

机构信息

Department of Anatomy and Developmental Biology, University College of London, England.

出版信息

Gastroenterology. 1993 Apr;104(4):1072-82. doi: 10.1016/0016-5085(93)90276-i.

Abstract

BACKGROUND

The effect of diabetes on the density of peptide-containing nerves in the pyloric sphincter of streptozotocin-induced diabetic rats and the possible preventive action of the ganglioside mixture AGF1 on the diabetes-induced changes were investigated.

METHODS

Immunohistochemical techniques were used to localize the general neuronal marker protein gene product 9.5 and the neuropeptides, calcitonin gene-related peptide, [met]-enkephalin, neuropeptide Y, substance P, and vasoactive intestinal polypeptide.

RESULTS

The density of neurones showing immunoreactivity to the above peptides in nerves supplying the thickened circular muscle layer of the pyloric sphincter was reduced extensively in diabetic rats. In the ganglioside-treated diabetic animals, this reduction was prevented; indeed, calcitonin gene-related peptide- and substance P-like immunoreactivity in the ganglioside-treated diabetic rats exceeded that seen in control animals. In the ganglioside-treated controls, there was no significant difference in the peptide immunoreactivity from that of untreated controls.

CONCLUSIONS

The results of the present study show that the ganglioside mixture AGF1 is effective in protecting the nerves of the pyloric sphincter from diabetes-induced changes.

摘要

背景

研究了糖尿病对链脲佐菌素诱导的糖尿病大鼠幽门括约肌中含肽神经密度的影响,以及神经节苷脂混合物AGF1对糖尿病诱导变化的可能预防作用。

方法

采用免疫组织化学技术定位一般神经元标记蛋白基因产物9.5以及神经肽、降钙素基因相关肽、[甲硫氨酸]脑啡肽、神经肽Y、P物质和血管活性肠多肽。

结果

糖尿病大鼠供应幽门括约肌增厚环形肌层的神经中,对上述肽显示免疫反应性的神经元密度显著降低。在经神经节苷脂治疗的糖尿病动物中,这种降低得到了预防;事实上,经神经节苷脂治疗的糖尿病大鼠中降钙素基因相关肽和P物质样免疫反应性超过了对照动物。在经神经节苷脂治疗的对照组中,肽免疫反应性与未治疗的对照组相比无显著差异。

结论

本研究结果表明,神经节苷脂混合物AGF1可有效保护幽门括约肌神经免受糖尿病诱导的变化。

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