Author + information
- Diao Jiayu and
- Jin Wei
To determine the effects of rosmarinic acid (RA) and STAT3 pathway on high glucose-induced mitochondrial and myocardiocyte injury in H9c2 cells and their mechanisms.
H9C2 cardiomyoctyes were randomly divided into normal-glucose group (NG), high-glucose group (HG), HG + RA groups (cells pretreatment with RA 5μM, 20μM, and 50μM). The reactive oxygen species (ROS) generation, the activation of mitochondrial permeability transition pore (MPTP), the levels of mitochondrial membrane potential (MTP), cell apoptotic rate and the expressions of cytochrome c, caspase-3 and STAT3 were detected.
Pretreatment with RA suppressed high glucose-induced apoptosis in H9c2 cells. RA improved mitochondrial function, which were demonstrated by attenuating high glucose-induced ROS generation, and suppressing the activation of MPTP, preserving the level of MTP and the release of cytochrome c and caspase-3 from mitochondrial in H9c2 myocardial cells. In addition, the greatest effect of RA was with 50μM. The activation of STAT3 was inhibited with high-glucose condition, but was reactivated by RA pretreatment. Inhibition the expression of STAT3 using STAT3-siRNA partly suppressed the effect on high glucose-induced apoptosis of RA.
Pretreatment with RA suppressed the high glucose-induced apoptosis in myocardial cells through improving mitochondrial function and activating the STAT3 signaling pathway.