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Gastroenterology Research and Practice
Volume 2014 (2014), Article ID 618068, 8 pages
http://dx.doi.org/10.1155/2014/618068
Research Article

Proanthocyanidin from Grape Seed Extracts Protects Indomethacin-Induced Small Intestinal Mucosal Injury

The Department of Internal Medicine, The Catholic University of Korea College of Medicine, St. Mary’s Hospital, Yeongdeungpo-gu 63-ro 10, Seoul 150-713, Republic of Korea

Received 5 February 2014; Revised 1 April 2014; Accepted 1 April 2014; Published 27 April 2014

Academic Editor: Paolo Gionchetti

Copyright © 2014 Dae Young Cheung et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Proanthocyanidin (grape seed proanthocyanidin extracts, GSPEs) is an antioxidant and scavenges free radicals. Excessive oxidative stress and free radical production are major components in the pathogenesis of NSAID-induced small intestinal injury. We investigated the effect of GSPEs on indomethacin-induced intestinal mucosal injury in the rat. Rats were allocated into four groups: the null control group, the indomethacin control group, the low-dose GSPEs group, and the high-dose GSPEs group. GSPEs were administered for 4 days. Then indomethacin and GSPEs were coadministered for the following 2 days by oral route. The dose of indomethacin was 200 mg/Kg. The doses of GSPEs were 100 mg/Kg for low-dose group and 300 mg/Kg for high-dose group. Luminal bleeding was solely observed in one of 5 rats from indomethacin control group. The number of ulcer count was reduced to 0.1 ± 0.3 per rat in GSPEs treated group compared to 1.4 ± 0.5 per rat in indomethacin control group. Submucosal inflammatory cell infiltration was also reduced to 50% in GSPEs treated group. The tissue level of prostaglandin E2 was not affected by GSPEs treatment. GSPEs attenuated the indomethacin-induced small intestinal injury irrespective of the tissue PGE2 depletion and glutathione consumption.