The Protective Effect of Fasudil on the Structure and Function of Cardiac Mitochondria from Rats with Type 2 Diabetes Induced by Streptozotocin with a High-Fat Diet Is Mediated by the Attenuation of Oxidative Stress
Figure 4
Effect of fasudil on cardiac Rho/ROCK activity. Levels of ROCK 1, ROCK 2, Rho A, and phosphorylated MYPT were detected in rat cardiac tissues using western blot analysis. (a) Representative results of assays of ROCK 1, ROCK 2, Rho A, and phospho-MYPT-1 and beta-actin abundances in rat cardiac tissues. (b) The levels of ROCK 1 protein expression were analyzed by western blot by using a polyclonal antibody to ROCK 1 to quantify its expressions in cardiac tissues. Data are expressed as the mean ± SD ( compared with untreated diabetic group). (c) The levels of ROCK 2 protein expression were analyzed by western blot by using a polyclonal antibody to ROCK 2 to quantify its expressions in cardiac tissues. Data are expressed as the mean ± SD ( compared with untreated diabetic group). (d) Average signal intensities quantified and expressed as percentage of the ratio of beta-actin to quantify Rho A expressions in cardiac tissues. Data are expressed as mean ± SD. The average signal intensities were significantly lower for diabetic rats treated with fasudil than for untreated diabetic rats (). (e) Average signal intensities quantified and expressed as a percentage of the ratio of T-MYPT to quantify levels of phosphorylated MYPT in cardiac tissues. Data are expressed as the mean ± SD. The ratio was significantly lower for diabetic rats treated with fasudil than for untreated diabetic rats (). (f) Five oxidative stress biomarkers were measured in heart tissues from diabetic-treated, untreated, and control rats. * versus control group. # versus untreated diabetic group.
