Paeonol improves angiotensin II-induced cardiac hypertrophy by suppressing ferroptosis

Canzhang Liu; Xin Yi; Jie Yan; Qiang Liu; Teng Cao; Shuipeng Liu

doi:10.1016/j.heliyon.2023.e19149

Paeonol improves angiotensin II-induced cardiac hypertrophy by suppressing ferroptosis

Heliyon. 2023 Aug 21;9(9):e19149. doi: 10.1016/j.heliyon.2023.e19149. eCollection 2023 Sep.

Authors

Canzhang Liu¹, Xin Yi¹, Jie Yan¹, Qiang Liu¹, Teng Cao¹, Shuipeng Liu²

Affiliations

¹ Department I of Cardiovasology, North China University of Science and Technology Affiliated Hospital, Tangshan City, Hebei Province, 063000, PR China.
² Department of Ultrasonic Medicine, North China University of Science and Technology Affiliated Hospital, Tangshan City, Hebei Province, 063000, PR China.

Abstract

The aim of this study was to investigate the protective effect of paeonol (pae) on an angiotensin II (AngII)-induced cardiac hypertrophy mouse model. First, AngII mouse models were constructed and randomly grouped into the control (con), AngII, and AngII + Pae groups. Compared with that in the blank group, the surface area of myocardial cells in the AngII group increased significantly. In contrast to that in the AngII group, the cardiomyocyte surface area in the Pae group was significantly reduced. Ultrasound results showed that the myocardial function of mice in the AngII group was decreased compared with that in the Con group, while the myocardial function of mice in the Pae treatment was significantly improved. Moreover, the Fe²⁺ and lipid peroxide levels of primary cardiomyocytes were significantly increased after treatment with AngII and were significantly decreased after the addition of Pae. Compared with those in the Con group, cristae were reduced and the outer membrane was lost in the myocardial tissues of the AngII group, and myocardial MDA, ROS, and Fe²⁺ levels were increased. However, myocardial damage was significantly alleviated after Pae treatment, and myocardial MDA, ROS, and Fe²⁺ levels were reduced. Moreover, in myocardial tissue, AngII reduced the protein levels of xCT and GPX4, while the levels of both xCT and GPX4 were increased after Pae treatment. In conclusion, Pae protected the hearts of AngII mice by upregulating the protein expression of xCT and GPX4 and resisting AngII-induced ferroptosis in cardiomyocytes.

Keywords: Angiotensin II; Cardiac hypertrophy; Ferroptosis; Paeonol; xCT/GPX4.