naloxone and Ulcer

Gastric ulcer induced by NSAIDs is the major medical concern and researchers are utilizing several approaches to combat this medical issue. In the current study, we investigated the efficacy of thiadiazinethione derivative (2,2'(2-thioxo-1,3,5-thiadiazinane-3,5-diyl) diacetic acid, as new less ulcerogenic compound.. 2,2'(2-thioxo-1,3,5-thiadiazinane-3,5-diyl) diacetic acid was evaluated using standard animal models including hot plate, writhing test and formalin induced nociceptive models. Anti-inflammatory activity was assessed via carrageenan-induced paw oedema model. Involvement of opioidergic nociceptive mechanism was confirmed via naloxone administration in hot plat assay. The gastro-ulcerogenic potential of test and standard compounds were evaluated via NSAID-induced pyloric ligation model followed by standard histopathological and biochemical analysis.. In acetic acid-induced writhing test, our compound significantly reduced abdominal constrictions at the tested doses of 15 (. Our findings suggests that our test compound has desirable anti-nociceptive and anti-inflammatory potentials with less propensity to cause gastric ulcer.

Topics: Analgesics; Animals; Anti-Inflammatory Agents; Anti-Inflammatory Agents, Non-Steroidal; Aspirin; Carrageenan; Edema; Formaldehyde; Naloxone; Stomach Ulcer; Tramadol; Ulcer

We studied the effect of parenteral morphine and naloxone administration on intestinal mucosal Prostaglandin E2 (PGE2) and 3',5' cyclic adenosine monophosphate (cAMP) levels and on indomethacin-induced intestinal ulceration in the rat. Compared to the control group, morphine significantly decreased whereas naloxone markedly increased both PGE2 and cAMP mucosal levels, respectively. Morphine or naloxone alone did not cause mucosal injury. However, when given with indomethacin, morphine significantly potentiated the ulcerogenic effect of indomethacin while naloxone exerted a protective effect. These results suggest that opioid peptides may play a role in modulation of intestinal mucosal PGE2 and cAMP levels. In addition, enhancement of indomethacin-induced ulcer formation by morphine and amelioration by naloxone might be in part mediated through their effect on mucosal PGE2 and cAMP levels.

Topics: Animals; Cyclic AMP; Dinoprostone; Indomethacin; Intestinal Mucosa; Intestine, Small; Male; Morphine; Naloxone; Narcotics; Rats; Rats, Inbred Strains; Ulcer

Naloxone, an opiate antagonist, was reported to protect against stress ulcers in dogs and rats. We studied its possible protective effect against indomethacin-induced intestinal ulceration in the rat. Naloxone was indeed found to possess a marked protective effect on the intestinal mucosa (ulcer index 73.3 +/- 13.6 vs. 273.8 +/- 21.8, p less than 0.001). Naloxone was found to elevate basal intestinal mucosal prostaglandin E2 (p less than 0.001) and cyclic adenosine monophosphate levels (p less than 0.005) but was unable to overcome the inhibition of prostaglandin E2 caused by indomethacin. An increase of cyclic adenosine monophosphate levels was seen, however, even in the presence of indomethacin, suggesting that cyclic adenosine monophosphate, but not prostaglandins, may play a role in the protective effect of naloxone.

Topics: Animals; Cimetidine; Cyclic AMP; Dinoprostone; Dose-Response Relationship, Drug; Indomethacin; Intestinal Diseases; Male; Naloxone; Prostaglandins E; Rats; Rats, Inbred Strains; Time Factors; Ulcer