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.