Pre-administration of turmeric prevents methotrexate-induced liver toxicity and oxidative stress.

BACKGROUND: Methotrexate (MTX) is an antimetabolite broadly used in treatment of cancer and autoimmune diseases. MTX-induced hepatotoxicity limits its application. We investigated hepatoprotective effects of turmeric in MTX-induced liver toxicity. METHODS: All experiments were performed on male Wistar albino rats that were randomly divided into six groups. Group one received saline orally for 30 days (control group), groups two and three received turmeric extract (100, 200 mg/kg respectively) orally for 30 days, group four received single dose, of MTX IP at day 30, groups five and six received turmeric extract 100 and 200 mg/kg orally respectively for 30 days and single dose of methoterxate IP (20 mg/kg) at day 30. Four days after MTX injection animals were sacrificed and evaluated. Blood ALT and AST (indicators of hepatocyte injury), ALP and bilirubin (markers of biliary function), albumin (reflect liver synthetic function) as well as the plasma TAS concentration (antioxidant defenses) were determined. The cellular antioxidant defense activities were examined in liver tissue samples using SOD, CAT, and GSH-Px for the oxidative stress, and MDA for lipid peroxidation. In addition, liver damage was evaluated histopathologically. RESULTS: MTX significantly induced liver damage (P<0.05) and decreased its antioxidant capacity, while turmeric was hepatoprotective. Liver tissue microscopic evaluation showed that MTX treatment induced severe centrilobular and periportal degeneration, hyperemia of portal vein, increased artery inflammatory cells infiltration and necrosis, while all of histopathological changes were attenuated by turmeric (200 mg/kg). CONCLUSION: Turmeric extract can successfully attenuate MTX-hepatotoxicity. The effect is partly mediated through extract's antinflammatory activity.

Protective effect of turmeric extract on ethotrexate-induced intestinal damage and oxidative stress.

AIM: The most important side effect of methotrexate (MTX) is mucositis. The purpose of this study was to evaluate the effect of turmeric extract on intestinal damage and oxidative stress in rats receiving methotrexate. METHODS: Experiments were performed on male Wistar albino rats divided into six groups. First group received normal saline orally, the second group received turmeric extract (100 mg·kg(-1)) orally for 30 days, the third group received turmeric extract (200 mg·kg(-1)) orally for 30 days, the fourth group received a single dose of methotrexate (20 mg·kg(-1)) i.p. at day 30, the fifth group received turmeric extract (100 mg·kg(-1)) orally for 30 days and a single dose of methotrexate (20 mg·kg(-1)) i.p. at day 30, and the sixth group received turmeric extract (200 mg·kg(-1)) orally for 30 days and single dose of methotrexate (20 mg·kg(-1)) i.p. at day 30. Four days after methotrexate injection, animals were anesthetized, blood samples were taken to determine total antioxidant status (TAS) and jejunum samples were taken for glutathione peroxidase (GPx), superoxidase dismutase (SOD), catalase (CAT), aldehyde malondialdehyde (MDA), and histopathological assessment. RESULTS: Microscopic evaluation from intestinal tissues of the MTX treated group, showed severe villus shortening and blunting, inflammatory cell infiltration and hemorrhage in lamina propria, along with epithlial cell necrosis. Levels of SOD, GSH-Px and CAT decreased in the MTX received group, but increased significantly (P < 0.05) in the turmeric + MTX groups. MTX increased lipid peroxidation, however, turmeric decreased peroxidation significantly (P < 0.05). CONCLUSION: These results suggest that turmeric extract may protect the small intestine of rats from methotrexate-induced damage. Turmeric effects could result from its antioxidant properties.

Comparative study of tomato and tomato paste supplementation on the level of serum lipids and lipoproteins levels in rats fed with high cholesterol.

BACKGROUND: Hypercholesterolemia is one of the risk factors of cardiovascular diseases. Increased blood cholesterol affects general health and increases mortality due to cardiovascular disease. Poor nutrition increases LDL cholesterol and decreases LDL receptor activities in the liver. Scientists have shown that consumption of antioxidants can reduce hypercholesterolemia and proved benefits of fruit and vegetables. Tomato reduces oxidative stress by increasing serum total antioxidant level. OBJECTIVES: This study compared the tomato and tomato paste supplementation on the level of serum lipids and lipoproteins in rats fed with high cholesterol. MATERIALS AND METHODS: In this study, four male rat groups (10 rats per group) were used. Control group received basal diet, second group received basal diet and 2% cholesterol (Chol), third and fourth groups received basal diet, 2% cholesterol tomato and tomato paste respectively (20 percent of the diet) for a month. Then serum TC, LDL, HDL and TG were measured. RESULTS: Results showed that in Chol group, all lipids increased significantly (P < 0.05) except HDL compared to the control group. Tomato and tomato paste supplementation decreased TC, LDL and TG concentration significantly (P < 0.05) compared to Chol group. Tomato paste had the higher effect on lipids decreasing than tomato. CONCLUSIONS: Decreases of TC, LDL and TG may be related to tomato antioxidant effect. This course in human required more investigations.