Gastric protection against cold restraint stress-induced lesions by amoxycillin in rats.

AIMS: Recent investigations have shown that amoxycillin possesses gastric protection properties in addition to its known antimicrobial effects. Therefore, this study was undertaken to investigate the potential gastric protection effects of amoxycillin and to determine its possible mechanism(s) of action in rats. METHODS: The cold restraint stress model was used to produce gastric mucosal lesions. The gastric secretion studies were undertaken by using Shay's pylorus ligation technique. The antioxidant effect was studied by luminol dependent chemiluminescence technique in vitro. RESULTS: Amoxycillin dose-dependently prevented cold restraint stress-induced mucus depletion and afforded protection. It inhibited indomethacin-stimulated gastric acid secretion with a high dose without affecting basal secretion. Furthermore, amoxycillin dose-dependently inhibited the phorbol myristate acetate-stimulated luminol-dependent chemiluminescence responses of isolated human poylmorphonuclear leukocytes in vitro. CONCLUSIONS: These results suggest that mechanisms of gastric protection effects of amoxycillin may include inhibition of stimulated acid secretion, prevention of depletion of mucus and antioxidant properties.

Natural honey exerts its protective effects against ethanol-induced gastric lesions in rats by preventing depletion of glandular nonprotein sulfhydryls.

The role of nonprotein sulfhydryls (NP-SH) in the protective effects of honey against absolute ethanol-induced gastric lesions was studied in rats. Sucralfate and ranitidine were used as known standard gastroprotective agents. Honey orally and drugs orally or subcutaneously were administered to 24 h fasted rats 30 or 90 min before oral administration of ethanol. Mucosal damage and the glandular NP-SH levels were measured 1 h after ethanol. Both honey and sucralfate dose-dependently afforded protection against gastric damage and reversed the changes in glandular NP-SH levels induced by ethanol. Ranitidine was ineffective in this model. Pretreatment with indomethacin (IND) did not alter the protective effects of honey or the NP-SH levels, but significantly reduced the protective effects of sucralfate. On the other hand, pretreatment with N-ethylmaleimide (NEM) significantly reduced the protective effects of both honey and sucralfate and lowered the NP-SH levels. Combined IND and NEM treatment caused a significant reduction of the protective effects of honey and the NP-SH levels, but the values were not significantly different from those obtained with NEM alone. In contrast, combined IND plus NEM treatment completely abolished the protective effects of sucralfate and significantly lowered the NP-SH levels. Although these results suggest the involvement of prostaglandins (PGs) -- sensitive process in the protective effects of sucralfate, but honey and sucralfate (partially) share a common mechanisms of action in mediating the gastroprotective effects through NP-SH sensitive processes.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibitory effect of natural honey on Helicobacter pylori.

Honey is widely used in folk-medicine throughout the world. However, it has a limited use in modern medicine due to lack of scientific support. Based on some recent reports, an in vitro study was undertaken to evaluate its antibacterial activity on Helicobacter pylori and a few other pathogenic organisms. All isolates of H. pylori were inhibited by 20 per cent of honey. Most of the other bacteria examined (including both Gram-positive and Gram-negative) were also inhibited at concentrations of 20 per cent of honey; and half of them were inhibited by 10 per cent of honey. Furthermore, it was observed that some isolates were resistant to various antimicrobial agents but honey inhibited these organisms and the sensitive ones equally. Our study advocates carrying out clinical investigation of the effect of honey on gastroduodenal disorders colonised by H. pylori.