Prdx1 overexpression inhibits oxidative stress through Nrf2 / HO-1 signaling pathway and reduces myocardial hypertrophy and fibrosis in spontaneously hypertensive rats
10.19405/j.cnki.issn1000-1492.2023.02.004
- Author:
Xinbo Ji
1
;
Shenhong Gu
1
;
Huade Mai
1
;
Biwei Fu
2
Author Information
1. Dept of General Medicine，The First Affiliated Hospital of Hainan Medical College，Haikou 570100
2. School of Basic Medicine and Life Sciences，Hainan Medical College，Haikou 571199
- Publication Type:Journal Article
- Keywords:
Prdx1;
spontaneous hypertension;
cardiac hypertrophy;
myocardial fibrosis;
oxidative stress;
Nrf2 / HO-1 signaling pathway
- From:
Acta Universitatis Medicinalis Anhui
2023;58(2):196-201
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of peroxide reductase 1 (Prdx1) on myocardial hypertrophy and fibrosis in spontaneously hypertensive rats，and to analyze its mechanism．
Methods:Forty five SHR rats were randomly divided into model group (SHR group) ，AAV9-NC group and AAV9-Prdx1 group．There were 15 WKY rats in each group，and the other 15 Wistar Kyoto rats were set as the control group．The rats in each group were administered continuously for 8 weeks，and the indexes of cardiac function were detected by echocardiography ; The mean blood pressure and myocardial hypertrophy were measured ; HE staining and Masson staining were used to observe the histomorphology and fibrosis of rat myocardium ; The indexes of oxidative stress in rat serum were detected by ELISA ; The expression level of Prdx1 mRNA in rat myocardium was detected by qRT-PCR ; Western blot was used to detect the expression of Prdx1 protein and nuclear factor E2 related factor 2 (Nrf2) / heme oxygenase-1 (HO-1) signaling pathway related proteins in rat myocardium.
Results: Compared with the Control group，the expression of Prdx1 mRNA and protein ，left ventricular ejection fraction ( EF) and left ventricular shortening rate ( FS) decreased in SHR group (P＜0. 05) ，the mean blood pressure，heart mass index ( HMI) and left ventricular mass index (LVMI) of rats increased (P＜0. 05) ，and there were obvious pathological damage and collagen fiber deposition in myocardial tissue．The activities of superoxide dismutase (SOD) and glutathione peroxidase ( GSH-Px) in rat serum decreased，and the content of malondialdehyde (MDA) increased (P＜0. 05) ; The expression of Nrf2， HO-1 and quinone oxidoreductase 1 (NQO1) protein decreased in myocardial tissue (P＜0. 05) ．Compared with SHR group，the expression of Prdx1 mRNA and protein，EF and FS in myocardial tissue of AAV9-Prdx1 group increased (P＜0. 05) ，the mean blood pressure，HMI and LVMI of rats decreased (P＜0. 05) ，and myocardial tissue injury and myocardial fibrosis improved ; The activities of SOD and GSH-Px in rat serum increased，while the content of MDA decreased (P＜0. 05) ; The expression of Nrf2，HO-1 and NQO1 protein increased in myocardial tissue (P＜0. 05) ．
Conclusion: Overexpression of Prdx1 can reduce myocardial hypertrophy and fibrosis and improve cardiac function in SHR rats．Its mechanism may be related to activating Nrf2 / HO-1 signaling pathway and inhibiting oxidative stress response.
- Full text:2024071322370368475Prdx1过表达通过Nrf...高血压大鼠心肌肥厚和纤维化_纪新博.pdf
