Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To better understand the mechanism of phosphatidylcholine synthesis in the stomach, [3H] choline incorporation into phosphatidylcholine in response to the drugs which have been commonly used for treating the patients with gastric ulcer was examined using isolated guinea pig gastric glands. Teprenone stimulated [3H] choline incorporation into phosphatidylcholine in gastric glands, up to 146 +/- 11% of control (n = 6, P less than 0.05). On the other hand famotidine, ranitidine and cimetidine significantly decreased the incorporation to 73 +/- 8%, 72 +/- 11%, 67 +/- 11% of control, respectively (n = 6, P less than 0.05, P less than 0.05, P less than 0.05). When the glands were pulsed with [3H] choline followed by incubation in the presence of teprenone or each H2RA for 180 min to see the effects of the agents on the limiting step of the phosphatidylcholine synthesis, teprenone also significantly stimulated [3H] choline incorporation into phosphatidylcholine, but each H2RA did not affect phosphatidylcholine biosynthesis any more. Teprenone stimulated CTP:phosphocholine cytidylyltransferase (CTF) from a basal value of 0.92 +/- 0.10 to 1.69 +/- 0.39 (nmol/min/mg protein) (n = 3, P less than 0.05). These results suggest that teprenone may stimulate phosphatidylcholine biosynthesis through the activation of CTF, a late-limiting enzyme of PC biosynthesis, and H2RA may affect phosphatidylcholine synthesis by inhibiting choline transport or choline kinase in gastric glands.
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PMID:[Effect of teprenone and H2-receptor antagonists on phosphatidylcholine synthesis in the isolated guinea pig gastric glands]. 197 87

Teprenone (Selbex), a gastric mucosal protective drug for treatment of chronic gastritis and gastric ulcer, has recently been used in the People's Republic of China. Teprenone in the treatment of chronic superficial gastritis (CSG): a surveillance study was recently conducted in 4 major hospitals in Beijing. The study included 98 patients (teprenone group 53 patients, Merzulene-S group 45 patients) with endoscopically proven gastritis. The study showed that teprenone may relieve symptoms of CSG in 8 weeks. The effectiveness rate for flatulence was 90.9% and for epigastralgia 87.2%. The improvement rate for the chronic inflammation in histopathology was 39.6% and disappearance rate for the activity of inflammation was 13.9%. It raised significantly the aminohexose level in gastric mucosa (P < 0.05) and increased gastric mucosal blood flow in gastric antrum (P < 0.05). These data suggest that teprenone is a safe and effective gastric mucosal protective drug.
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PMID:[Teprenone in the treatment of chronic superficial gastritis, a multicentre study]. 927 38

Teprenone, an anti-ulcer drug, has been reported to promote the healing of acetic acid-induced chronic gastric ulcers in rats by stimulating gastric mucus synthesis and secretion. Recently, it has been implicated that neutrophil infiltration and lipid peroxidation in ulcerated gastric tissues have an inhibitory effect on the healing of acetic acid-induced chronic gastric ulcers in rats. Therefore, we attempted to clarify whether teprenone exerts a healing-promoting effect on acetic acid-induced chronic gastric ulcers through its inhibitory effect on neutrophil infiltration and lipid peroxidation in ulcerated gastric tissues. In rats with chronic gastric ulcers made by applying acetic acid to the stomach, gastric ulcer healing started later than 3 days after the acetic acid application. Gastric mucosal myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration, and lipid peroxide content were higher in the ulcerated region than in the intact region on the 8th, 15th, and 22nd day after the acetic acid application. Gastric mucosal non-protein SH content was lower in the ulcerated region than in the intact region on the 8th, 15th, and 22nd day after the acetic acid application, and gastric mucosal adherent mucus content was lower in the ulcerated region than in the intact region on the 8th and 15th day. Daily oral administration of teprenone (100 mg kg(-1)x 2) for 7 or 14 days, starting on the 8th day after the application of acetic acid to the stomach, enhanced the reduction of the ulcer area with attenuation of all these biochemical changes found in the ulcerated region. The teprenone administration caused a decrease in MPO activity and an increase in adherent mucus content in the gastric mucosa of the intact region. These results suggest that the healing-promoting effect of teprenone on acetic acid-induced chronic gastric ulcers in rats could be due not only to stimulation of gastric mucus secretion but also to inhibition of neutrophil infiltration and enhanced lipid peroxidation in the ulcerated gastric tissue.
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PMID:Teprenone promotes the healing of acetic acid-induced chronic gastric ulcers in rats by inhibiting neutrophil infiltration and lipid peroxidation in ulcerated gastric tissues. 1120 62