Objective To investigate the changes of mitochondrial membrane potential and cardiomyocyte apoptosis as welll as the intervention of telmisartan, further to explore whether telmisartan can improve cardiomyocyte apoptosis through the possible pathway of mitochondria correlated in diabetic rats.
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. After 12 weeks, Fluorescent probe DCFH-DA was used to monitored the levels of reactive oxygen species and JC-1 was used to monitored the changes of mitochondrial membrane potential by spectrofluorophotometer. Cardiomyocyte apoptosis was evaluated by TUNEL.
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). Compared with controls, Body weight decreased remarkably in DM group and T group (410.63±11.59 vs 426.88±14.32, p<0.01). Cardiomyocyte apoptosis was seen few in control group; compared with control group, cardiomyocyte apoptotic index ascended (0.35±0.16 vs 0.15±0.08, p<0.05) and mitochondrial membrane potential (ΔΨm) depressed (9.66±1.70 vs 19.88±1.38, p<0.01) in DM group, but the index of cardiomyocyte apoptosis was lower (0.17±0.08 vs 0.35±0.16, p<0.05) and transmembrane potential (ΔΨm) (16.84±1.84 vs 9.66±1.70, p<0.01) in T group was higher than that of DM group.
Conclusion Telmisartan can promote mitothondrial membrane potential and improve cardiomyocyte apoptosis in type 1 diabetic rats.