PMID- 10489873 OWN - NLM STAT- MEDLINE DCOM- 19991025 LR - 20190915 IS - 0253-6269 (Print) IS - 0253-6269 (Linking) VI - 22 IP - 4 DP - 1999 Aug TI - Effect of DA-6034, a derivative of flavonoid, on experimental animal models of inflammatory bowel disease. PG - 354-60 AB - Inflammatory bowel disease (IBD) is a multifactorial disorder with unknown etiology and pathogenesis. DA-6034, 7-carboxymethyloxy-3', 4', 5-trimethoxy flavone, is a synthetic flavonoid known to possess anti-inflammatory activity. This study was performed to evaluate the oral therapeutic effect of DA-6034 in three experimental animal models of IBD: two chemical-induced IBD models of rats and the human leukocyte antigen (HLA)-B27 transgenic rat model known to develop spontaneous colitis without the use of exogenous agents. Acute chemical colitis was induced by intracolonic instillation of 1.2 ml of 4% acetic acid solution. Prednisolone (1 mg/kg), sulfasalazine (100 mg/kg) and DA-6034 (0.3 to approximately 3 mg/kg) were orally administered twice daily for 6 days in these rats. In addition, chronic chemical colitis was induced by intracolonic administration of trinitrobenzene sulfonic acid (TNBS) 30 mg in 50% ethanol and agents were orally administered for 6 or 20 days. In chemical-induced IBD models, all of these agents reduced the severity of colitis and specially, DA-6034 (3 mg/kg) showed more potent effect than other drugs in macroscopic lesion score. In HLA-B27 transgenic rats, DA-6034 (3 mg/kg) and prednisolone (0.5 mg/kg) were treated orally twice daily for 6 weeks. The HLA-B27 transgenic rats showed only mild colitis, compared with the chemical-induced colitis models. DA-6034 ameliorated the loose stool and decreased microscopic damage, which is the important indicator of this model. In conclusion, oral therapy of DA-6034 attenuated the macroscopic and histologic damages of the colon in all three experimental models of IBD, which suggest that DA-6034 could be a promising drug in the treatment of IBD. FAU - Kim, Y S AU - Kim YS AD - Department of Internal Medicine, Seoul National University, College of Medicine, Korea. FAU - Son, M AU - Son M FAU - Ko, J I AU - Ko JI FAU - Cho, H AU - Cho H FAU - Yoo, M AU - Yoo M FAU - Kim, W B AU - Kim WB FAU - Song, I S AU - Song IS FAU - Kim, C Y AU - Kim CY LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - Korea (South) TA - Arch Pharm Res JT - Archives of pharmacal research JID - 8000036 RN - 0 (Anti-Inflammatory Agents) RN - 0 (Anti-Inflammatory Agents, Non-Steroidal) RN - 0 (Flavonoids) RN - 0 (Gastrointestinal Agents) RN - 0 (HLA-B27 Antigen) RN - 0 (beta 2-Microglobulin) RN - 3XC8GUZ6CB (Sulfasalazine) RN - 8T3HQG2ZC4 (Trinitrobenzenesulfonic Acid) RN - 9PHQ9Y1OLM (Prednisolone) RN - Q40Q9N063P (Acetic Acid) RN - U96J5LG435 (recoflavone) SB - IM MH - Acetic Acid MH - Animals MH - Animals, Genetically Modified MH - Anti-Inflammatory Agents/therapeutic use MH - Anti-Inflammatory Agents, Non-Steroidal/*pharmacology MH - Colitis/chemically induced/drug therapy MH - Flavonoids/*pharmacology MH - Gastrointestinal Agents/therapeutic use MH - HLA-B27 Antigen/genetics/immunology MH - Humans MH - Inflammatory Bowel Diseases/chemically induced/*drug therapy/pathology MH - Organ Size/drug effects MH - Prednisolone/therapeutic use MH - Rats MH - Sulfasalazine/therapeutic use MH - Trinitrobenzenesulfonic Acid MH - Weight Loss/drug effects MH - beta 2-Microglobulin/genetics/immunology EDAT- 1999/09/18 00:00 MHDA- 1999/09/18 00:01 CRDT- 1999/09/18 00:00 PHST- 1999/09/18 00:00 [pubmed] PHST- 1999/09/18 00:01 [medline] PHST- 1999/09/18 00:00 [entrez] AID - 10.1007/BF02979057 [doi] PST - ppublish SO - Arch Pharm Res. 1999 Aug;22(4):354-60. doi: 10.1007/BF02979057.