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KMID : 0881720160310040286
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Journal of Food Hygiene and Safety
2016 Volume.31 No. 4 p.286 ~ p.293
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Protective Effects on Gastric Lesion of Ursolic acid
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Kim Sun-Whoe
Hwang In-Young
Lee Sun-Yi
Jeong Choon-Sik
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Abstract
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This study is an experiment for gastric protective effects of ursolic acid. In order to identify the effects of ursolic acid on gastrointestinal disorder, acute and chronic gastritis were also observed using HCl·ethanol and indomethacin-induced gastric lesion models, respectively. As for gastric acid, it was also identified through proton pump (H+/K+-ATPase) inhibiting activity. In regards to protective factor for gastric damage, prostaglandin E2 (PGE2) was quantitatively analyzed. Antibacterial activity experiment was done on Helicobacter pylori (H.pylori), which is known to be the causing factor of chronic gastritis, gastric ulcer and gastric cancer. By making use of AGS cell, it was confirmed that ursolic acid was involved in apoptosis of gastric cancer cell through 4’,6-diamidino-2-phenylindol (DAPI) staining and flow cytometry analysis. As a result, ursolic acid reduced gastric lesions caused by HCl·ethanol and indomethacin. Ursolic acid inhibited acid secretion by inhibiting proton pump (H+/K+-ATPase), which is the gastric acid secreting enzyme involved at the final phase of gastric acid secretion. And ursolic acid was identified with gastric mucosa protection effects by increasing the concentration of PGE2, a protective factor of gastric mucosa preservation. The antibacterial activity on H. pylori, which is aggressive factor in gastrointestinal disorder, ursolic acid showed inhibitory effects on H. pylori colonization. In the DAPI nuclear staining, unlike the control group, shape of the nucleus has deformed, and has been observed either shrinked cell or chromatin condensation phenomenon. In the Flow cytometry assay, confirmed the growth rate of apoptosis in a concentration-dependent manner.
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KEYWORD
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H+/K+-ATPase, PGE2, H. pylori, Apoptosis
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