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The effects of apigenin-7-O-β-d-glucuronopyranoside on reflux oesophagitis and gastritis in rats

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1 This study evaluated the inhibitory action of apigenin-7-O-β-d-glucuronopyranoside (AGC), apigenin, and omeprazole on reflux oesophagitis and gastritis in rats. AGC was isolated from Clerodendron trichotomum leaves.

2 Oesophagitis and gastritis were induced by surgical procedure and the administration of indomethacin, respectively. The intraduodenal (i.d.) administration of AGC decreased the volume of gastric juice and increased the gastric pH compared with apigenin and omeprazole. The acid output was more inhibited by AGC in a dose-dependent manner than by apigenin and omeprazole. Compared with apigenin and omeprazole, AGC significantly decreased the size of gastric lesions, which were induced by exposure of the gastric mucosa to indomethacin.

3 Malondialdehyde (MDA) content, which is the end product of lipid peroxidation, was increased significantly after the induction of reflux oesophagitis. The MDA content was decreased by AGC (i.d. 3 mg kg−1), but not by either apigenin or omeprazole. This suggests that AGC has an antioxidative effect. In the oesophagitis group, the mucosal levels of glutathione (GSH) were significantly lower than that in the normal group. However, the GSH levels were preserved after administering the AGC, suggesting that AGC possesses scavenging activity.

4 In summary, AGC is more potent than apigenin and omeprazole at inhibiting reflux oesophagitis and gastritis and may therefore be a promising drug for their treatment.

Keywords: AGC; apigenin; free radical; gastric secretion; lipid peroxidation; omeprazole; rat; reflux oesophagitis

Document Type: Research Article


Affiliations: 1: Pharmacology 2: Pharmaceutical Botany, College of Pharmacy, Chung Ang University, Seoul 156-756, Korea

Publication date: July 1, 2005

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