Original Article
Copyright ©2012 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Apr 7, 2012; 18(13): 1479-1484
Published online Apr 7, 2012. doi: 10.3748/wjg.v18.i13.1479
Curcumin prevents indomethacin-induced gastropathy in rats
Duangporn Thong-Ngam, Sakonwan Choochuai, Suthiluk Patumraj, Maneerat Chayanupatkul, Naruemon Klaikeaw
Duangporn Thong-Ngam, Sakonwan Choochuai, Suthiluk Patumraj, Maneerat Chayanupatkul, Department of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
Naruemon Klaikeaw, Department of Pathology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand
Author contributions: Thong-Ngam D designed the study, performed the experiments, analyzed the data, and wrote the manuscript; Choochuai S performed the experiments and collected the data; Patumraj S provided analytical tools; Chayanupatkul M analyzed data and edited the manuscript; Klaikeaw N coordinated the pathological examination.
Supported by The Grant of Ratchadaphiseksomphot, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand [RA 53/52(2)]
Correspondence to: Duangporn Thong-Ngam, MD, Associate Professor, Department of Physiology, Faculty of Medicine, Chulalongkorn University, Bangkok 10330, Thailand. dr.duangporn@gmail.com
Telephone: +662-256-42672050 Fax: +662-256-42672823
Received: March 22, 2011
Revised: February 9, 2012
Accepted: February 16, 2012
Published online: April 7, 2012

AIM: To investigate the effects of curcumin on gastric microcirculation and inflammation in rats with indomethacin-induced gastric damage.

METHODS: Male Sprague-Dawley rats were randomly divided into three groups. Group 1 (control group, n = 5) was fed with olive oil and 5% NaHCO3- (vehicle). Group 2 [indomethacin (IMN) group, n = 5] was fed with olive oil 30 min prior to indomethacin 150 mg/kg body weight (BW) dissolved in 5% NaHCO3- at time 0th and 4th h. Group 3 (IMN + Cur group, n = 4) was fed with curcumin 200 mg/kg BW dissolved in olive oil 0.5 mL, 30 min prior to indomethacin at 0th and 4th h. Leukocyte-endothelium interactions at postcapillary venules were recorded after acridine orange injection. Blood samples were determined for intercellular adhesion molecule (ICAM)-1 and tumor necrosis factor (TNF)-α levels using enzyme linked immunosorbent assay method. Finally, the stomach was removed for histopathological examination for gastric lesions and grading for neutrophil infiltration.

RESULTS: In group 2, the leukocyte adherence in postcapillary venules was significantly increased compared to the control group (6.40 ± 2.30 cells/frame vs 1.20 ± 0.83 cells/frame, P = 0.001). Pretreatment with curcumin caused leukocyte adherence to postcapillary venule to decline (3.00 ± 0.81 cells/frame vs 6.40 ± 2.30 cells/frame, P = 0.027). The levels of ICAM-1 and TNF-α increased significantly in the indomethacin-treated group compared with the control group (1106.50 ± 504.22 pg/mL vs 336.93 ± 224.82 pg/mL, P = 0.011 and 230.92 ± 114.47 pg/mL vs 47.13 ± 65.59 pg/mL, P = 0.009 respectively). Pretreatment with curcumin significantly decreased the elevation of ICAM-1 and TNF-α levels compared to treatment with indomethacin alone (413.66 ± 147.74 pg/mL vs 1106.50 ± 504.22 pg/mL, P = 0.019 and 58.27 ± 67.74 pg/mL vs 230.92 ± 114.47 pg/mL, P = 0.013 respectively). The histological appearance of the stomach in the control group was normal. In the indomethacin-treated group, the stomachs showed a mild to moderate neutrophil infiltration score. Gastric lesions were erosive and ulcerative. In rats treated with indomethacin and curcumin, stomach histopathology improved and showed only a mild neutrophil infiltration score and fewer erosive lesions in the gastric mucosa.

CONCLUSION: The results indicate that curcumin prevents indomethacin-induced gastropathy through the improvement of gastric microcirculation by attenuating the level of ICAM-1 and TNF-α.

Keywords: Curcumin, Nonsteroidal anti-inflammatory drugs, Gastric damage, Gastric microcirculation, Intercellular adhesion molecule-1, Tumor necrosis factor-α