When ‘ + 1′ score is assigned to the control tissue sections, ACB stained piroxicam treated animal tissue sections scored ‘ + 3′. Such observation revealed a pathological change in mucin secretion type on piroxicam treatment. The histopathological finding clearly indicates that piroxicam treatment increases acid mucin secretion in otherwise neutral mucin secreting normal gastric tissue. Reduction in

ACB staining intensity in tissue sections from only Cu LE treated group indicates that mucin secretion pattern did not alter significantly selleck chemicals llc on pre-treatment with the extract. The free neutral mucin content depletes appreciably and the nature of secreted mucin turns acidic on ulcerated stomach. Figure 3D shows that piroxicam also mediates its ulcerative damage through reduction in mucin level by Crizotinib mouse 22.3% (*P≤ 0.001 Vs control). Cu LE pre-treated piroxicam fed animals had no such reduction in mucin content clearly indicating protection from ulcerative damage rendered

by the pre-feeding of the extract. Biomarkers of oxidative stress include lipid peroxidation level, protein carbonyl content, reduced glutathione (GSH), non enzymatic total sulfhydryl group content (TSH), oxidized glutathione (GSSG) content and GSH-GSSG ratio. Table 1 represents the changes in biomarkers of oxidative stress on piroxicam treatment and protection rendered on pre-treatment of rats with Cu LE at a dose of 200 mg/kg body weight. Lipid peroxidation level and protein carbonyl content increased in piroxicam treated rats by 2.16 folds and 5.57 folds respectively, compared to values obtained (P≤0.001Vs

control) in control rats. Levels of TSH and GSH decreased significantly in piroxicam fed rats by 59.17% and 59.63% respectively from control rats (*P ≤ 0.001 Vs control in each case). GSSG content increased by 51.16% and the ratio (GSSG: GSH) increased by 4.3 folds from control in piroxicam treated rats (*P≤0.001 Vs control in each case). Values in the table ID-8 no.1 clearly indicate that no biomarkers altered on feeding rats with only aqueous extract of curry leaves at 200 mg/kg BW dose. Table 1 further indicate that altered biomarkers were restored to control values when rats were pre-treated with aqueous curry leaf extract at 200 mg/kg BW dose before feeding piroxicam at 30 mg/kg BW dose. Table 2 depicts the alterations in activities of different gastric antioxidant enzymes on piroxicam administration. Piroxicam feeding inhibits activities of key gastric antioxidant enzyme called gastric peroxidise and glutathione–S-transferase. Increased activities of gastric glutathione reductase, glutathione peroxidise, superoxide dismutases (Cu-Zn SOD and Mn SOD) and catalase are also observed on piroxicam feeding. Pre-treatment of piroxicam fed rats with Cu LE protected the activity of these antioxidant enzymes from being altered.