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Updated: Jan 27, 2026

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Published on: January 15, 2022
PDCD4 expression in coronary atherosclerosis rat models and its mechanism
Yuhong Gao1, Hongmei Li1, Yanchun Zhou2
1Department of Cardiology, Yidu Central Hospital of Weifang, Weifang, Shandong 262500, P.R. China.
Abstract:
This study investigated the expression of programmed cell death protein 4 (PDCD4) in rat models of coronary atherosclerosis (AS) and analyzed its role and mechanism. A total of 80 Wistar rats were selected and divided into the control group (n=40) and research group (n=40) according to the principle of similar body weight, of which coronary AS models were established in rats in the research group. PDCD4 expression in coronary artery tissues was detected using western blotting, and the expression of interleukin-6 (IL-6) and IL-8 in the coronary artery tissues were measured by means of reverse transcription-polymerase chain reaction (RT-PCR). The apoptotic rate of coronary artery smooth muscle cells was determined via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). The relative expression of PDCD4 in coronary artery tissues in the research group was obviously higher than that in the control group, and the difference was statistically significant (t=6.121, P<0.01). In terms of the relative expression of messenger ribonucleic acid (mRNA) of IL-6 in the coronary artery tissues, the research group had a remarkably higher level than the control group, with a statistically significant difference (t=21.03, P<0.01). The difference in the relative expression of IL-8 mRNA between the research group and the control group was statistically significant, of which a much higher level was detected in the research group (t=19.96, P<0.01). The apoptotic rate of smooth muscle cells in the research group was increased notably compared with that in the control group, and the difference was statistically significant (t=5.985, P<0.01). PDCD4 may participate in the formation of coronary AS plaque, and its possible function in the process is to inhibit the proliferation of vascular smooth muscle cells and promote the upregulation of IL-6 and IL-8.
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