Objective To investigate the level of oxidative stress in streptozotocin-induced type 1 diabetic rats as well as the intervention effects of telmisartan.
Methods Diabetic rat models were established by intraperitoneal injection of streptozotocin on adult male Wistar rats. The model diabetic rats were randomly divided into two groups of diabetic rats (DM group) and diabetic rats treated with telmisartan (T group) that was with eight in each group. There are eight normal rats as the control group (Con group). After 12 weeks, Body weight and heart weight were measured to calculate HW/BW. Lipid Peroxidation (Malondialdehyde, MDA), glutathione (GSH), the activity of superoxide dismutase (SOD) were evaluated by spectrophotometer. Ultra-microstructure of cardiac muscle cell and structure of heart was observed by transmission electron microscope.
Results The blood glucose were found no significant difference between those diabetic rats with and without telmisartan treatment groups at the 7th day after streptozotocin injection and the 12th week, but both higher than that of control group (p<0.01). The level of MDA in DM group was higher (6.92±0.62 vs 3.66±0.51, p<0.01) and the level of GSH was lower (7.88±1.76 vs 11.97±1.15, p<0.01) than those in Con group. The activity of SOD was also lower than those in Con group (155.35±17.23 vs 219.72±22.39, p<0.01). Compared with DM group, the level of GSH (11.22±1.67 vs 7.88±1.76, p<0.01) and the activity of SOD (187.70±20.59 vs 155.35±17.23, p<0.01) increased remarkably in T group, meanwhile, the level of MDA in T group was lower than that of DM group (4.24±0.47 vs 6.92±0.62, p<0.01). Myocardium of DM group was characterised by mitochondrial swelled and crista mitochondriales arranged irregularly or broken even dissolved. In addition, vacuolar degeneration was observed obviously in mitochondria of myocardium. Injury change of ultramicrostructure of myocardium in T group Lessen obviously than DM group.
Conclusion Telmisartan may inhibit oxidative stress, then improves ultramicrostructure of myocardium in type 1 diabetic rats.