Abstract
Background and Aims Hydrotalcite plays an important role in the therapy of gastric ulcer induced by nonsteroidal anti-inflammatory drugs (NSAIDs), but little is known about the mechanism. We designed two experiments to study the preventive and curative effects of hydrotalcite on NSAIDs-related gastric injury in rats and to investigate the relationship between the protective and curative mechanism of hydrotalcite and the secretion of epidermal growth factor (EGF)/prostaglandin E2 (PGE2). Methods Two experiments were separately designed to evaluate the preventive and curative effects of hydrotalcite. A total of 25 male rats and 25 female rats were randomly divided into five groups (vehicle group, model group, omeprazole group, hydrotalcite group, and ranitidine group) in each experiment. Rats were treated with indomethacin by gavage to build the model of acute gastric mucosal injury. The concentrations of EGF and PGE2 in blood specimens and mucosal injury indexes by gross inspection were measured and an immunohistochemical technique was also employed to test the levels of EGF, cyclooxygenase-1 (COX-1), and cyclooxygenase-2 (COX-2) in gastric mucosa. Results Comparing with model group in both preventive and curative experiments, hydrotalcite decreased the gastric injury in the mucosa of stomach significantly (7±4.5 vs. 16±11.25, 1.5±2 vs. 2.5±6; P<0.01, P<0.05). The levels of EGF and PGE2 in blood serum were markedly higher in hydrotalcite group than that in model group and ranitidine group in preventive experiment (574.39±34.28 vs. 486.22±41.73, 488.07±24.44; P<0.01, P<0.01). The expression levels of COX-2 in gastric mucosa were also higher in hydrotalcite group than that in model group in both preventive and therapeutic experiments (12±4 vs. 9±6, 14±7 vs. 9±4; P<0.01, P<0.05). Conclusions Hydrotalcite promotes gastric protection and healing via several mechanisms, including increased levels of PGE2 in blood serum, activation of EGF, and antagonising the inhibition of cyclooxygenase (COX) caused by NSAIDs.
Highlights
Nonsteroidal anti-inflammatory drugs (NSAIDs) have been widely used in clinical fields characterized by antiinflammatory, pain-relief, antiplatelet aggregation, and antithrombogenesis [1]
After 24h of food starvation, animals were treated with indometacin (30mg/kg dissolved in ddH2O) by gavage to establish the model of acute gastric mucosal injury as previously described
Our results showed that the expression of prostaglandin E2 (PGE2) in each drug-treated group was increased in both experiments, and the expression of PGE2 in hydrotalcite group was significantly increased compared with model group in preventive experiment, suggesting that hydrotalcite enhances PGE2 expression in the mucosal blood to protect and heal gastric mucosal injury
Summary
Nonsteroidal anti-inflammatory drugs (NSAIDs) have been widely used in clinical fields characterized by antiinflammatory, pain-relief, antiplatelet aggregation, and antithrombogenesis [1] In recent years, these drugs have been applied to prevent tumors by stimulation of apoptosis and inhibition of cell proliferation [2, 3]. We designed two experiments to study the preventive and curative effects of hydrotalcite on NSAIDs-related gastric injury in rats and to investigate the relationship between the protective and curative mechanism of hydrotalcite and the secretion of epidermal growth factor (EGF)/prostaglandin E2 (PGE2). The levels of EGF and PGE2 in blood serum were markedly higher in hydrotalcite group than that in model group and ranitidine group in preventive experiment (574.39±34.28 vs 486.22±41.73, 488.07±24.44; P
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