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- Title
Stachydrine ameliorates hypoxia reoxygenation injury of cardiomyocyte via enhancing SIRT1-Nrf2 pathway.
- Authors
Zhu, Xi; Wu, Yingbiao; Zhang, Xiaogang; Gu, Wei; Ning, Zhongping
- Abstract
Background: Hypoxia/reoxygenation (H/R)-induced cardiomyocyte cell apoptosis is critical in developing myocardial infarction. Stachydrine (STA), an active constituent of Leonurus heterophyllus sweet, could have a protective effect on myocardial H/R injury, which remains unexplored. Therefore, the study aimed to investigate the protective effects and mechanisms of STA on H/R injury of cardiomyocytes. Methods: Rat cardiomyocyte H9c2 cells underwent H/R (hypoxia for 4 h and reoxygenation for 12 h). Cells were pretreated with STA (50 µM) 2 h before H/R. Cardiomyocyte injury was evaluated by CCK-8 assay and lactate dehydrogenase (LDH) release. Apoptosis was assessed by TUNEL staining and caspase-3 activity. Oxidative stress was assessed by lipid oxidation product MDA and a ROS-scavenging enzyme SOD in culture media. Western blot was performed to measure the protein expressions of SIRT1, Nrf2, and heme oxygenase-1 (HO-1). Results: STA reversed the decrease in cell viability and increased LDH release in H9c2 cells with the H/R insult. STA significantly suppressed oxidative stress, reduced MDA content, and increased SOD activity in H9c2 cells exposed to H/R. STA reduced apoptosis in H9c2 cells exposed to H/R, as evidenced by the reduced TUNEL positive cells and caspase-3 activity. In addition, STA enhanced SIRT1, Nrf2, and HO-1 protein expression in H/R-stimulated H9c2 cells. SIRT1 and Nrf2 involved the protective effect of STA in H/R-exposed H9c2 cells, as the changes in cell viability and caspase-3 activity by STA can be reversed by SIRT1 inhibitor EX-527 or Nrf2 siRNA. Conclusions: Our data speculated that STA protects H/R injury and inhibits oxidative stress and apoptosis in cardiomyocytes by activation of the SIRT1-Nrf2 pathway.
- Subjects
SIRTUINS; HYPOXEMIA; LACTATE dehydrogenase; WOUNDS &; injuries; PROTEIN expression
- Publication
Journal of Cardiothoracic Surgery, 2023, Vol 18, Issue 1, p1
- ISSN
1749-8090
- Publication type
Article
- DOI
10.1186/s13019-023-02363-6