Famotidine-induced suppression of gastric surface mucus cell function is prevented by combined treatment with MMSC, raising the possibility of a more effective cure of PUD.
COX-2 is an inducible cyclooxygenase (COX) that has been reported to be expressed in the macula densa and surrounding cortical thick ascending limb in normotensive rats. The present study assessed the contribution of COX-2 in three different rat models of hypertension, each characterized by a different activation of the renal renin-angiotensin system. Mean blood pressure (MBP) in the rat 2 kidney-1 clip (2K1C) model was significantly reduced with a COX-2 selective inhibitor, NS-398 (10 mg/kg, p.o., twice a day) (vehicle-administered rats (n = 8): 154 +/- 6 mmHg; NS-398-administered rats (n = 5): 128 +/- 10 mmHg). By contrast, a COX-1 selective inhibitor, mofezolac, did not lower MBP. Increased plasma renin activity (23 +/- 8 ng/kg/h (n = 6) vs. sham operation, 2.4 +/- 0.9 ng/kg/h (n = 4)) was markedly reduced to 6.8 +/- 2.7 ng/ml/h (n = 5) by NS-398, but not by mofezolac. The development of 1 kidney-1 clip (1K1C) hypertension was also inhibited by NS-398 (vehicle (n = 12): 133 +/- 1 mmHg; NS-398 (n = 7): 122 +/- 3 mmHg) accompanied by a reduction in plasma renin activity (3.0 +/- 0.3 ng/ml/h, n = 4) to 1.0 +/- 0.2 ng/ml/h (n = 5). The COX-2 inhibitor increased urinary excretions in the 1K1C model, but not in the 2K1C model. In a deoxycorticosterone acetate (DOCA)-salt model, plasma renin activity was markedly suppressed to less than 0.3 ng/ml/h. The COX-2 inhibitor caused no significant changes in MBP, plasma renin activity, or urinary excretion, suggesting that COX-2 made a lesser contribution in this model. Increased expression of COX-2 mRNA and protein was observed in the kidneys of 1K1C and 2K1C rats, but not in DOCA-salt rats. These results suggest that COX-2 plays a significant role in the development of 2K1C and 1K1C renovascular hypertension, in addition to making a substantial contribution to the diuretic effect in the 1K1C model.
it has been recognized that distinct mucus secreting cells of the gastrointestinal tract express specific type of tnucins. We have recently demonstrated that a kind of sialomucin specifically stained with a monoclonal antibody (mAb) HCl\/I31 is temporarily and specifically expressed in the mucous cells regenerated from acetic acid-induced gastric damage in rats. The aim of this study was to iinmunohistochemically characterize the distribution of the specific type of sialomucins recognized by this mAb throughout the digestive tract and age-dependent alteration of this expression in rats. The gastrointestinal tracts of eight-week-old and eighty-eight-week-old male Sprague Dawley rats were used in this study. In both young and aged rats, HCM3l reacted with the surface mucous cells of the cardiac gland, recognizable as 2 or 3 pits adjacent to the forestomach. The goblet cells in the duodenum, jejunum, ileum, cecum and proximal colon were also stained with HCM3l. In the young rat, epithelial cells including the goblet cells in the distal colon and the rectum were not stained with HCM3l. On the other hand, the goblet cells in the distal colon and rectum of the aged rats were stained positively with HCM3l. These findings indicate that the immunohistocliemical observations using this n1Ab, as well as other anti-mucin mAbs developed by us, should be very useful for the evaluation of changes in the mucin species with respect to the physiological and pathological alterations in the alimentary tract of rats.It has been recognized that distinct inucus-secreting cells of the gastrointestinal tract express a specific type of mucin (1, 2, '7, 12). For example, the surface mucous cells and the mucous neck cells of the rat corpus mucosa synthesize and secrete a distinct type of mucins stained with anti-mucin monoclonal antibodies (mAbs) RGM2l and HIKl083, respectively. We have recently demonstrated that a kind of stalotnucin specifically stained with HCM3l (an antimucin mAb developed by us) is temporarily and specifically expressed in the mucous cells regenerated from acetic acid-induced gastric damage in rats (4). This mAb was developed by immunizing a mouse with mucins purified from resected human colonic mucosa as an immunogen. Although an irnmunohistochemical characterization of this mAb has been well established in human gastrointestinal tracts, staining of HCM3l was not well understood in the rat digestive tract. In this study, we sought mucus secreting cells positively stained with this rnAb throughout the gastrointestinal mucosa of normal
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