期刊
NEUROGASTROENTEROLOGY AND MOTILITY
卷 25, 期 7, 页码 -出版社
WILEY-BLACKWELL
DOI: 10.1111/nmo.12122
关键词
diabetes; M2 macrophage; oxidative stress
资金
- JSPS Bilateral Joint Projects with Belgium (FWO) [11035231-000061]
- JSPS Bilateral Joint Projects with Korea (NRF) [12032211-000109]
- Research Fund of Mitsukoshi Health and Welfare Foundation
- MEXT
- Smoking Research Foundation
- Keio Gijuku Academic Development Funds
- [24659103]
- Grants-in-Aid for Scientific Research [24659103] Funding Source: KAKEN
Background Streptozotocin (STZ) is known to induce type I diabetes and the loss of the interstitial cells of Cajal (ICC). However, the regulation of heme oxygenase-1 (HO-1) expression, which is reported to protect ICC, has not yet been elucidated in this model. The aim of this study was to investigate the alterations of HO-1 expression and clarify the mechanism of ICC loss in the stomach using the rat model of STZ-induced diabetes. Methods Streptozotocin (65mgkg-1) was intraperitoneally administered to 8-week-old female Wistar rats. Cobalt protoporphyrin (CoPP), an HO-1 inducer, was administered subcutaneously once a week after the STZ injection. The expressions of HO-1 and the receptor tyrosine kinase c-Kit (a marker for ICC) proteins were investigated by western blot analysis and immunofluorescence staining. Key Results Expression of c-Kit, particularly in the gastric antrum, was significantly decreased at 8weeks, not at 1week, compared to those of the control group. Significantly increased induction of HO-1 expression, especially in the gastric corpus but not in the antrum, was observed in the STZ group at 8weeks after the STZ injection relative to control. CoPP administration significantly up-regulated HO-1 expression in the STZ diabetic group and significantly restored the previously reduced ICC in the gastric antrum. Conclusions & Inferences Up-regulation of HO-1 expression in the STZ diabetic model was limited to the gastric corpus and impaired up-regulation of HO-1 expression in the gastric antrum likely induced the disruption of the ICC network.
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