The role of fish oil in attenuating cardiac oxidative stress, inflammation and fibrosis in rat model of thyrotoxicosis.

Hyperthyroidism is associated with cardiovascular complications. Fish oil reduces risk of cardiovascular diseases. This study aims to evaluate the impact of fish oil on myocardial oxidative stress, inflammation and fibrosis in rat model of thyrotoxicosis. Rats were randomized into four groups; control rats, fish oil treated rats (FO, 100mg omega-3/100g body weight/day), hyperthyroid rats (Hyper, i.p levothyroxine 3 mg/kg/day), and hyperthyroid rats treated with fish oil (Hyper + FO) for 8 weeks. Changes in oxidants/antioxidants, inflammatory and fibrotic markers were measured. Thyrotoxicosis increased serum endothelin-1, thiobarbituric acid reactive substances (TBARS) and reduced activities of cardiac catalase and super oxide dismutase (SOD). Cardiac fibrosis paralleled with a decrease of matrix metalloproteinase -2 (MMP2) levels were observed in Hyper group. Use of FO increased activities of SOD and catalase, increased TBARS levels, and attenuated cardiac fibrosis by normalizing MMP-2 levels. Use of FO may attenuate cardiac oxidative stress and fibrosis in hyperthyroid states.

Cardiac effects of cigarette tobacco smoking in rat model of diabetes.

AIMS: Tobacco smoking is considered a global health issue, contributing to increased risk of cardiovascular disease (CVD) and diabetes (DM). We aimed to assess effects of cigarette smoking on cardiac inflammation, oxidative stress and fibrosis in rat model of streptozotocin (STZ)-induced diabetes. MAIN METHODS: Adults Wistar rats were assigned into control (fresh air, intraperitoneal injection (i.p) of citrate buffer), cigarette smoking (1 h daily for 4 weeks, i.p citrate buffer), DM (35 STZ mg/kg single i.p, fresh air), and DM + Smoking groups for 4 weeks. Cardiac biomarkers of oxidative stress, inflammation, and fibrosis were evaluated. KEY FINDINGS: STZ-induced diabetes as documented by the persistent increase in blood glucose. Relative to control, a significant decrease in body weight was observed in diabetic groups paralleled with increased heart to body weight ratio and systolic blood pressure in all groups. Levels of total nitrite, thiobarbituric acid substances, endothelin -1, interleukin-6 and myeloperoxidase were increased in the DM, Smoking and DM + Smoking groups without changes in C-reactive protein. Cardiac levels of GSH were increased in Smoking groups whereas activities of catalase and superoxide dismutase increased in DM, Smoking and DM + Smoking groups. DM but not smoking increased cardiac fibrosis with a parallel increase in transforming growth factor beta. Cardiac levels of matrix metalloproteinase-2 were elevated in Smoking groups and decreased in DM. SIGNIFICANCE: Exposure to cigarette smoke may increase risk of CVD in DM by increased cardiac oxidative stress and inflammation. Smoking was associated with increased oxidant enzymes and metalloproteinase-2 probably to prevent cardiac fibrosis.

Cardiac effects of fish oil in a rat model of streptozotocin-induced diabetes.

BACKGROUND AND AIMS: Fish oil (FO) is rich in omega-3 polyunsaturated fatty acids, which have cardio-protective effects. This study aims to evaluate effects of FO in a rat model of streptozotocin (STZ) induced diabetes. METHODS AND RESULTS: Adults male Wistar rats were assigned to control (4 µl corn oil/g corn oil given by oral gavage), FO (4 µl Menhaden FO/g body weight given by oral gavage), diabetes (DM, 35 mg/kg STZ single intraperitoneal injection, corn oil), and DM + FO groups for 8 weeks. Plasma and cardiac biomarkers of oxidative stress, inflammation, and fibrosis were evaluated. STZ-induced diabetes as indicated by the significant increase in serum levels of glucose and percentage of glycated hemoglobins. FO reduced plasma arachidonic acid (AA) percentage and ratio of AA: docosahexaenoic acid (DHA). Plasma and cardiac levels of total nitrite, endothelin -1 (ET-1), and myeloperoxidase (MPO) increased in the DM group, whereas cardiac activities of catalase and superoxide dismutase (SOD) decreased. FO reduced cardiac nitrite and MPO, and plasma ET-1 levels. FO increased cardiac glutathione, catalase and SOD activities. Levels of thiobarbituric acid substances increased in the FO and DM groups with significant synergism in the DM + FO group. FO prevented cardiac fibrosis associated with DM and decreased cardiac transforming growth factor beta-1and p38 MAP kinases. Cardiac levels of matrix metalloproteinase -2 were significantly elevated in FO and DM + FO groups. CONCLUSIONS: FO decreased plasma and cardiac oxidative stress, inflammation and myocardial fibrosis. FO could be used in diabetes to reduce risk and burden of CVDs.