Drugs online research references
Phytother Res. 2001 Nov;15(7):625-7.
Antiulcerogenic effect of Hippophae rhamnoides L.
Suleyman H, Demirezer LO, Buyukokuroglu ME, Akcay MF, Gepdiremen A, Banoglu ZN, Gocer F.
Ataturk University, Faculty of Medicine, Department of Pharmacology, Erzurum, Turkey.
The antiulcerogenic effect of a hexane extract (HRe-1) from Hippophae rhamnoides (Eleagnaceae) was tested on indomethacin- and stress-induced ulcer models. As a result HRe-1 was found to be active in preventing gastric injury. Copyright 2001 John Wiley & Sons, Ltd.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11746847&dopt=Abstract
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Br J Pharmacol. 2001 May;133(1):37-42.
Mobilization of rat stomach ECL-cell histamine in response to short- or long-term treatment with omeprazole and/or YF 476 studied by gastric submucosal microdialysis in conscious rats.
Konagaya T, Bernsand M, Norlen P, Hakanson R.
Department of Pharmacology, Institute of Physiological Sciences, University of Lund, Solvegatan 10, S-223 62 Lund, Sweden.
1. Mobilization of histamine from the ECL cells was monitored by gastric submucosal microdialysis in conscious rats. The ECL cells are known to operate under gastrin control and the purpose of the present study was to examine their in situ response to short-term (12 h) as well as long-term (28 days) hypergastrinaemia, induced by treatment with the proton pump inhibitor omeprazole. 2. Hypergastrinaemia promptly raised the histamine concentration in the microdialysate. The effect was prevented by CCK(2) receptor blockade (YF476). On day 7 of omeprazole treatment the microdialysate histamine concentration reached a peak, five times higher than before treatment. Subsequently (14 and 28 days), less histamine was mobilized. 3. Gastrin infusion (4 h) raised the microdialysate histamine concentration in a dose-dependent manner in fasted rats and freely fed rats and in rats treated with omeprazole for a week. However, while fasted and fed rats responded to low doses of gastrin, the omeprazole-treated rats required large doses of gastrin to respond. 4. When the amount of histamine mobilized was related to the serum gastrin concentration the following EC(50) values could be calculated: fasted rats 2.3 x 10(-10) M, freely fed rats 2.5 x 10(-10) M, omeprazole-treated rats 8.7 x 10(-10) M. The maximal histamine responses in the three groups were 18.4 pmol 4 h(-1)+/-0.8, 21.9 pmol 4 h(-1)+/-1.2 and 68.0 pmol 4 h(-1)+/-3.5, respectively. 5. The results suggest that ECL cells, exposed to a high gastrin concentration for a week, respond with a shift in the receptor-ligand binding affinity from high to low. Apparently, CCK(2) receptors of the ECL cells are subject to dynamic changes with respect to ligand-binding affinity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11325792&dopt=Abstract
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mb.kyoto-phu.ac.jp
BACKGROUND/AIM: We examined the healing process of chronic gastric ulcers in adjuvant-induced arthritic rats and investigated the mechanism for delayed ulcer healing in arthritic rats, in relation to acid secretion and basic fibroblast growth factor (bFGF). METHODS: Arthritis was induced in male dark Agouti rats by a single injection of Freund's complete adjuvant (FCA), while gastric ulcers were induced by thermal cauterization (70 degrees C for 30 s) 7 days after FCA injection. RESULTS: Injection of FCA induced severe arthritis in all animals with a marked acid hypersecretion. The healing of gastric ulcers was significantly delayed in arthritic rats as compared with normal rats. Daily administration of indomethacin delayed ulcer healing in both normal and arthritic rats, but this effect was more pronounced in the latter. In contrast, the healing of gastric ulcers was significantly promoted in both normal and arthritic rats by omeprazole at a dose that inhibited acid secretion completely. The delayed healing of gastric ulcers was not influenced by twice daily administration of N(G)-nitro-L-arginine methyl ester, aminoguanidine or FR167653 (IL-1/TNF-alpha synthesis inhibitor), but was significantly accelerated by CS-23 (recombinant human bFGF) in a dose-dependent manner, without effect on the acid secretion. The expression of bFGF was markedly increased after ulceration, but this response was decreased in arthritic rats. CONCLUSION: The healing of gastric ulcers was delayed in arthritic rats, and this mechanism may be partly attributable to both acid hypersecretion and less expression of bFGF. Copyright 2001 S. Karger AG, Basel
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11351144&dopt=Abstract
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