Please use this identifier to cite or link to this item: http://scholarbank.nus.edu.sg/handle/10635/107491
Title: Calcitonin gene-related peptide protects cultured rat gastric mucosal cells
Authors: Tu, Y. 
Kang, J.-Y. 
Keywords: Calcitonin gene-related peptide
Capsaicin
Cultured gastric mucosal cells
Substance P
Issue Date: 1998
Source: Tu, Y.,Kang, J.-Y. (1998). Calcitonin gene-related peptide protects cultured rat gastric mucosal cells. European Journal of Gastroenterology and Hepatology 10 (4) : 317-324. ScholarBank@NUS Repository.
Abstract: Capsaicin exerts its gastroprotective effect by stimulating primary afferent neurons, releasing calcitonin gene-related peptide (CGRP), which in turn increases gastric blood flow. In this work, the effects of capsaicin, rat α-CGRP, and relative peptides hCGRP8-37 and β-hCGRP, and substance P on cultured gastric mucosal cells independent of neural and vascular mechanisms were studied. Damage was produced by indomethacin, ethanol or taurocholate 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenybromide and trypan blue exclusion tests were used to assess viability of the cultured cells. Capsaicin administration alone did not injure gastric cells. However, capsaicin pretreatment potentiated the damaging effect of indomethacin and ethanol. In the sodium taurocholate model, capsaicin slightly protected the cells against injury, α-rCGRP was protective against indomethacin, ethanol and taurocholate in a dose-dependent manner, hCGRP8-37 and β-hCGRP both dose-dependently prevented injury caused by indomethacin at concentrations about eight times higher than that of α-rCGRP, but substance P was ineffective in the three different damage models. A combination of α-CGRP and hCGRP8-37 was also protective against indomethacin damage to a similar extent as use of either agent alone. The defence mechanism of capsaicin against gastric cell injury may in part be mediated by a direct effect of CGRP on gastric mucosal cells, in addition to effects dependent on neural and vascular mechanisms, hCGRP8-37 has no antagonist effect against CGRP in this model, suggesting that CGRP receptors in this model may be different from those in other tissues.
Source Title: European Journal of Gastroenterology and Hepatology
URI: http://scholarbank.nus.edu.sg/handle/10635/107491
ISSN: 0954691X
Appears in Collections:Staff Publications

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