Objective: To investigate the correlation between the endothelial cell apoptosis and sirtuin-3 (SIRT3) gene expression in atherosclerosis (AS) rats.
Materials and methods: The AS model in rats was established through the high-fat diet. A total of 12 rats fed normally were enrolled as the control group, while 12 rats fed with high-fat diet were enrolled as the experimental group. After the experiment, the aortic tissues of rats were collected, and the relative area of the arterial plaque (total area of plaque/total area of the vessel) was measured via oil red O staining. The serum was collected to detect the levels of blood lipid, including total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C). Moreover, the expression levels of SIRT3 and apoptotic genes were determined via Reverse Transcription-Polymerase Chain Reaction (RT-PCR), Western blotting and immunohistochemistry (IHC), respectively. The apoptosis was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining.
Results: The area of aortic plaque in the experimental group [(36.15±9.52)%] was significantly larger than that in the control group [(11.62±3.25)%] (p<0.01). Compared with those in the control group, the serum TC, TG and LDL-C levels were significantly increased in the experimental group, while the HDL-C level was significantly decreased (p<0.05). Compared with those in the control group, the mRNA and protein expression levels of SIRT3 in the aorta of rats markedly declined in the experimental group (p<0.05), while Caspase-3 and Caspase-9 expressions were significantly increased (p<0.05), respectively. The results of TUNEL staining revealed that the apoptosis in the aorta of rats in the experimental group was remarkably higher than that in the control group (p<0.05).
Conclusions: The expression of SIRT3 is deleted in the aorta of AS rats and closely related to the apoptosis. SIRT3 may serve as a potential target for the treatment of AS.