| Objective To study the effects of low expression of protein NDUFS4 on mitochondria function of ventricular myocytes in the neonatal rats. Methods The ventricular myocytes following primary culture derived from 30 neonatal rats were randomly divided into two groups. The ventricular myocytes in the siRNA treatment group were transinfected by NDUFS4 siRNA, and those in the control group were transinfected by nonsense siRNA. After further culture for 48 hours, the expression of NDUFS4 protein, potential of mitochondrial membrane, level of cellular reactive oxygen species (ROS), capacity of calcium intake of mitochondria, and respiratory control ratio (RCR) of mitochondria between the cells of two groups were compared. Results In comparison with the ventricular myocytes of neonatal rats in the control group, expression of NDUFS4 protein in the ventricular myocytes of siRNA treatment group reduced by 73.58% (P<0.001), potential of mitochondrial membrane reduced by 20.49% (P<0.05), but level of cellular ROS increased by 32.11% (P<0.001). Furthermore, calcium intake capacity of mitochondria in the siRNA treatment group reduced by 33.33% (P<0.001), and maximal velocity of cellular respiration reduced by 29.18% (P<0.05), more than those in the control group. Conclusion Expression of protein NDUFS4 may play an important role in the stabilization of mitochondria membrane potential, formation of cellular ROS, opening of mitochondrial permeability transition pore (MPTP), and maintenance of energy supply in the mitochondria of ventricular myocytes of neonatal rats. |
