Atractylodesin III maintains mitochondrial function and inhibits caspase-3 activity to reverse apoptosis of cardiomyocytes in AMI rats

The aim of the present study was to analyze the effects of Atractylodesin III (codonopsis pilosula) extract that maintains mitochondrial function, up-regulates Bcl-2, inhibits Caspase-3 activity, and ultimately leads to cardiomyocyte apoptosis in a rat model of acute myocardial infarction (AMI). 30 male Sprague-Dawley rats aged 6 months, weighed 150-200 g were randomly divided into sham operation group (SOG), model group (MG) and intervention group (IG). The IG was intragastrically administered with atractylodesin III (30 mg/kg/d) for 7 days. The model group was treated with (30 mg/kg/d) of sterile saline. After 4.5 h, the heart samples from each group were taken, the myocardial infarct size was detected by 2, 3, 5-triphenyltetrazolium chloride (TTC) staining.After ematoxylin & Eosin (HE) staining apoptosis indices were determined by Terminal deoxynucleotidyl transferase TdT-mediated dUTP Nick-End Labeling (TUNEL) method. Apoptosis-related genes and protein including Bcl-2, Bax, and Caspase-3 expression were determined by quantitative real time polymerase chain reaction (qRT-PCR) and western blot respectively. The infarct size and apoptotic index of the MG were significantly higher than SOG. However, infarct size and apoptotic index were reduced in IGcompared to MG (P < 0.05). The levels of Bax and Caspase-3 in the MG were significantly higher, while Bcl-2 and Bcl-2/Bax were lower than those in the SOG. The IG has lower levels of Bax and Caspase-3, higher levels of Bcl-2 and Bcl-2/Bax (P < 0.05) compared to MG. Atractylodesin III decreased apoptosis of myocardial cells in AMI, up-regulated Bcl-2 expression, and inhibited Bax and Caspase-3 activity.