title: Curcumin reduces indomethacin-induced damage in the rat small intestine.
abstract: Non-steroidal anti-inflammatory drugs (NSAIDs) are commonly used in clinical medicine. Their utility is, however, often limited by the adverse effects they produce in the gastrointestinal tract. Oxidative stress has been shown to occur in the small intestine in response to the oral administration of indomethacin, an NSAID commonly used in toxicity studies. In view of this, the effect of curcumin, an agent with anti-oxidant properties, was evaluated on indomethacin-induced small intestinal damage in a rat model. Rats were pretreated with various doses of curcumin (20 mg kg(-1), 40 mg kg(-1) and 80 mg kg(-1)) before administering indomethacin at 20 mg kg(-1). Various parameters of oxidative stress and the extent of small intestinal damage produced by indomethacin, with and without pretreatment with curcumin, were measured. Macroscopic ulceration was found to occur in the small intestine in response to indomethacin. The viability of enterocytes from indomethacin-treated animals was significantly lower than those from control animals. Drug-induced oxidative stress was also evident as seen by increases in the levels of malondialdehyde and protein carbonyl and in activities of pro-oxidant enzymes such as myeloperoxidase and xanthine oxidase in indomethacin-treated rats. Concomitant decreases were seen in the activities of the antioxidant enzymes catalase and glutathione peroxidase in these animals. Pretreatment with curcumin was found to ameliorate these drug-induced changes. Thus, curcumin appears to hold promise as an agent that can potentially reduce NSAID-induced small intestinal damage.
authors.affiliation: Department of Biochemistry, Christian Medical College, Vellore-632002, Tamil Nadu, India.
authors.forename: Nageswaran
authors.initials: N
authors.lastname: Sivalingam
authors.forename: Raghunath
authors.initials: R
authors.lastname: Hanumantharaya
authors.forename: Minnie
authors.initials: M
authors.lastname: Faith
authors.forename: Jayasree
authors.initials: J
authors.lastname: Basivireddy
authors.forename: K A
authors.initials: KA
authors.lastname: Balasubramanian
authors.forename: Molly
authors.initials: M
authors.lastname: Jacob
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D020169:Caspases / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D002470:Cell Survival / Q000187:drug effects; D003474:Curcumin / Q000494:pharmacology* / Q000627:therapeutic use; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D004381:Duodenal Ulcer / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D020895:Enterocytes / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D005979:Glutathione Peroxidase; D007213:Indomethacin; D007421:Intestine, Small / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D009195:Peroxidase / Q000378:metabolism; D050050:Protein Carbonylation / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D014969:Xanthine Oxidase / Q000378:metabolism
chemical_list: D000975:Antioxidants; D008315:Malondialdehyde; D002374:Catalase; D009195:Peroxidase; D005979:Glutathione Peroxidase; D014969:Xanthine Oxidase; D020169:Caspases; D003474:Curcumin; D007213:Indomethacin