title: Mechanism of action of celecoxib on normal and acid-challenged gastric mucosa.
abstract: Selective COX-2 inhibitor, celecoxib, delays the healing of gastric ulcers by inhibiting prostaglandins synthesis. Therefore, the effect of celecoxib on normal and acid-challenged gastric mucosa was studied. Wistar rats were distributed into four groups: group-1 (vehicle treated), group-2 (celecoxib treated), group-3 (given 0.6N HCl) and group-4 (HCl+celecoxib treated). The gastric mucosa was assessed histopathologically and by evaluating gastric adherent mucus. To assess the role of oxidative stress, the levels of free radicals and antioxidants were measured. The histopathological examination showed mild inflammation in group-2, moderate inflammation in group-3 and severe inflammation in group-4. The results showed an increase in malondialdehyde and a decrease in gastric adherent mucus, nitrite, reactive thiols and glutathione in groups-2-4 as compared to control group. Activity of superoxide dismutase, catalase and glutathione-s-transferase was increased in all the groups except the group-1. The present study suggested that celecoxib aggravated the gastric damage caused by acid which may be mediated by altering the balance between free radicals and antioxidants.
authors.affiliation: Department of Biochemistry, Panjab University, Chandigarh, India.
authors.forename: Nisha
authors.initials: N
authors.lastname: Dutta
authors.forename: Pooja
authors.initials: P
authors.lastname: Sarotra
authors.forename: Shikha
authors.initials: S
authors.lastname: Gupta
authors.forename: Ritu
authors.initials: R
authors.lastname: Aggarwal
authors.forename: Navneet
authors.initials: N
authors.lastname: Agnihotri
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D000068579:Celecoxib; D052246:Cyclooxygenase 2 Inhibitors / Q000009:adverse effects*; D005753:Gastric Mucosa / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D005756:Gastritis / Q000139:chemically induced* / Q000201:enzymology / Q000378:metabolism / Q000473:pathology; D005978:Glutathione / Q000378:metabolism; D005982:Glutathione Transferase / Q000378:metabolism; D006851:Hydrochloric Acid; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009573:Nitrites / Q000032:analysis; D011720:Pyrazoles / Q000009:adverse effects*; D051381:Rats; D017208:Rats, Wistar; D013438:Sulfhydryl Compounds / Q000378:metabolism; D013449:Sulfonamides / Q000009:adverse effects*; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D052246:Cyclooxygenase 2 Inhibitors; D009573:Nitrites; D011720:Pyrazoles; D013438:Sulfhydryl Compounds; D013449:Sulfonamides; D008315:Malondialdehyde; D002374:Catalase; D013482:Superoxide Dismutase; D005982:Glutathione Transferase; D005978:Glutathione; D000068579:Celecoxib; D006851:Hydrochloric Acid