The protective mechanisms of paracetamol against ethanol-induced gastric mucosal damage in rats

Abstract

The protective mechanisms of paracetamol against ethanol-induced gastric mucosal damage have been examined. The antiulcer action of subcutaneously (s.c.)-injected paracetamol, 250 mg kg-1, was attenuated by either subdiaphragmatic vagotomy or s.c. injection of N-ethylmaleimide, 10 mg kg-1. This attenuation was not seen in rats given paracetamol by the oral route (p.o.). Indomethacin pretreatment, 5 mg kg-1, did not influence the lesion-preventing action of paracetamol given s.c. or p.o. The findings suggest that the antiulcer effect of s.c.-administered paracetamol results from an action involving the vagal nerve and tissue sulfhydryls, but not prostaglandins. On the other hand, the protective mechanism of paracetamol p.o. is independent of the vagal system or tissue sulfhydryls and prostaglandins. It seems that paracetamol given p.o. exerts its antiulcer effect by acting directly on the mucosal cell to strengthen mucosal integrity.

Protective Effect of Acetaminophen against Acute Gastric Mucosal Lesions Induced by Ischemia-Reperf usion in the Rat

“…This effect is con sistent with previous studies showing that ac etaminophen protected the gastric mucosa against various gastric irritants [21][22][23]. Sev eral mechanisms have been proposed for the protection of gastric mucosa by acetamino phen.…”

“…Sev eral mechanisms have been proposed for the protection of gastric mucosa by acetamino phen. For example, in gastric lesions induced by the water immersion restraint stress meth od, acetaminophen was thought to protect the gastric mucosa by inhibiting the reduction in gastric PGE2 levels [4,24] or to stimulate PGEi synthesis in the gastric mucosa [25], However, in some studies, acetaminophen failed to increase PGE2 content but enhanced gastric secretion of mucus or directly pro tected the gastric epithelial cells, independent of PG synthesis [3,6,23]. Thus, gastric pro tection by acetaminophen is not attributable to a single mechanism.…”

Cigarette smoking: Effects on P selectin expression and subsequent inflammatory responses in ethanol‐induced gastric mucosal damage

“…Lesion areas were measured with a grid (each grid square was 1 mm 2 ) by a person who was unaware of the treatment conditions. The total lesion areas were divided by the number of rats in each group and expressed as the mean lesion area 14 . The gastric glandular mucosae were scraped with a glass slide while on top of an ice‐cold dish.…”