Inhibitory effects of PGA1 and TRI on the apoptosis of cardiac microvascular endothelial cells of rats

Peng,Wen-Hua; Wang,Jia-Li; Ren,Yan; Gao,Yan-Xiang; Li,Geng; Wang,Yong

doi:10.3892/etm.2017.5079

Inhibitory effects of PGA1 and TRI on the apoptosis of cardiac microvascular endothelial cells of rats

Authors:
- Wen-Hua Peng
- Jia-Li Wang
- Yan Ren
- Yan-Xiang Gao
- Geng Li
- Yong Wang
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Affiliations: Department of Cardiology, China-Japan Friendship Hospital, Beijing 100029, P.R. China
Published online on: August 30, 2017 https://doi.org/10.3892/etm.2017.5079
Pages: 4288-4292
Copyright: © Peng et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

The present study investigated the protective effects and molecular mechanism of prostaglandin A1 (PGA1) and triptolide (TRI) on apoptosis of cardiac microvascular endothelial cells (CMVECs) in rats. CMVECs of rats were isolated and then cultured. MTT method was used to select and establish a cell hypoxia reoxygenation cell model. The cells were divided into four groups: Normoxia control group (C, normal oxygen), hypoxia reoxygenation group (H/R, hypoxia for 12 h/reoxygenation for 6 h), PGA1 group (H/R+PGA1) and TRI group (H/R+TRI). The growth of cells in each of the group was observed. B-cell lymphoma 2 (Bcl-2) mRNA expression in CMVECs and expression of Bcl-2 mRNA after PGA1 and TRI treatment were determined by RT-PCR. Cell apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay. Bcl-2 mRNA decreased significantly after hypoxia stimulation of CMVECs of rats. The expression of Bcl-2 mRNA was significantly higher in comparison to hypoxia stimulation group after treatment with PGA1 and TRI (P<0.01). The elevated effect of PGA1 on Bcl-2 mRNA was stronger than that of the TRI group (P<0.05). The number of CMVECs reduced significantly after hypoxia. By contrast, DNA fragmentation and the number of endothelial cell apoptosis were increased significantly. However, Bcl-2 mRNA expression decreased significantly, after PGA1 and TRI treatments. Furthermore, the number of apoptotic cells reduced and Bcl-2 mRNA expression increased (P<0.01). PGA1 and TRI significantly upregulated the expression of Bcl-2 mRNA, inhibited the activation of CMVECs and were able to achieve the protective effect on apoptosis of CMVECs in hypoxia‑oxygenated rats.

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