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Proanthocyanidin from grape seed extracts protects indomethacin-induced small intestinal mucosal injury.

Cheung DY, Kim JI, Park SH, Kim JK - Gastroenterol Res Pract (2014)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: 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.

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 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.

No MeSH data available.


Related in: MedlinePlus

Microscopic findings in the rat small intestine. (a) and (b) Erosions induced by indomethacin showed focal villous necrosis and reduced epithelial height. (c) and (d) Ulcers induced by indomethacin showed deep excavation of mucosa and exposed submucosal layer. Marked inflammatory cell infiltration was noted in the submucosal space. (e) and (f) Transmural inflammatory infiltration was present beyond the ulcer formation (hematoxylin-eosin stain, ×40).
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fig2: Microscopic findings in the rat small intestine. (a) and (b) Erosions induced by indomethacin showed focal villous necrosis and reduced epithelial height. (c) and (d) Ulcers induced by indomethacin showed deep excavation of mucosa and exposed submucosal layer. Marked inflammatory cell infiltration was noted in the submucosal space. (e) and (f) Transmural inflammatory infiltration was present beyond the ulcer formation (hematoxylin-eosin stain, ×40).

Mentions: Histological evaluation was performed on the proximal 5.0 cm segment of duodenum and proximal jejunum and distal 5.0 cm segment of ileum. The intestinal segments were immediately immersed in 10% formalin solution and fixed for 24 hours. Formalin-fixed intestines were longitudinally sliced into 2.0 mm wide segments and processed into paraffin blocks. Mounted tissue slides were stained with hematoxylin-eosin. Histological findings of mucosal damage were assessed by an independent pathologist blinded to treatment, according to the following criteria (Figure 2):


Proanthocyanidin from grape seed extracts protects indomethacin-induced small intestinal mucosal injury.

Cheung DY, Kim JI, Park SH, Kim JK - Gastroenterol Res Pract (2014)

Microscopic findings in the rat small intestine. (a) and (b) Erosions induced by indomethacin showed focal villous necrosis and reduced epithelial height. (c) and (d) Ulcers induced by indomethacin showed deep excavation of mucosa and exposed submucosal layer. Marked inflammatory cell infiltration was noted in the submucosal space. (e) and (f) Transmural inflammatory infiltration was present beyond the ulcer formation (hematoxylin-eosin stain, ×40).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4020456&req=5

fig2: Microscopic findings in the rat small intestine. (a) and (b) Erosions induced by indomethacin showed focal villous necrosis and reduced epithelial height. (c) and (d) Ulcers induced by indomethacin showed deep excavation of mucosa and exposed submucosal layer. Marked inflammatory cell infiltration was noted in the submucosal space. (e) and (f) Transmural inflammatory infiltration was present beyond the ulcer formation (hematoxylin-eosin stain, ×40).
Mentions: Histological evaluation was performed on the proximal 5.0 cm segment of duodenum and proximal jejunum and distal 5.0 cm segment of ileum. The intestinal segments were immediately immersed in 10% formalin solution and fixed for 24 hours. Formalin-fixed intestines were longitudinally sliced into 2.0 mm wide segments and processed into paraffin blocks. Mounted tissue slides were stained with hematoxylin-eosin. Histological findings of mucosal damage were assessed by an independent pathologist blinded to treatment, according to the following criteria (Figure 2):

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: 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.

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 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.

No MeSH data available.


Related in: MedlinePlus