Protective effects of epigallocatechin-3-gallate counteracting the chronic hypobaric hypoxia-induced myocardial injury in plain-grown rats at high altitude

• Published in: Cell stress & chaperones Vol. 28; no. 6; pp. 921 - 933
• Main Authors: Chen, Haotian, Chen, Chen, Qin, Yuhui, Wang, Lei, Zheng, Jie, Gao, Fabao
• Format: Journal Article
• Language: English
• Published: Dordrecht Springer Science + Business Media 01-11-2023; Springer Netherlands; Springer Nature B.V
• Subjects: Altitude; Apoptosis; Biochemistry; Biomedical and Life Sciences; Biomedicine; Blood; Cancer Research; Cell Biology; Enzymes; Epigallocatechin gallate; Heart; Heme oxygenase (decyclizing); High altitude; High-altitude environments; Hypoxia; Immunology; Inflammation; Inflammatory response; Magnetic resonance; Myocardium; Neurosciences; Original; ORIGINAL ARTICLE; Oxidative stress; Serum levels; Side effects; Structure-function relationships; Ventricle; Antioxidants; High altitude; Oxidative stress; Hypoxia; EGCG; Myocardial injury
• ISSN: 1355-8145; 1466-1268
• DOI: 10.1007/s12192-023-01386-1

Exposure to hypobaric hypoxia (HH) environment causes stress to the body, especially the oxygen-consuming organs. Chronic HH conditions have adverse effects on the myocardium. Thus, we conducted this experiment and aim to evaluate such adverse effects and explore the therapeutic role of epigallocatechin-3-gallate (EGCG) in rats’ heart under chronic HH conditions. For that purpose, we transported rats from plain to a real HH environment at high altitude for establishing the HH model. At high altitude, animals were treated with EGCG while the salidroside was used as the positive control. General physiological data were collected, and routine blood test results were analyzed. Cardiac magnetic resonance (CMR) was examined to assess the structural and functional changes of the heart. Serum levels of cardiac enzymes and pro-inflammatory cytokines were examined. Oxidative markers in the left ventricle (LV) were detected. Additionally, ultrastructural and histopathological changes and apoptosis of the LV were assessed. Furthermore, the antioxidant stress-relevant proteins nuclear factor E2-related factor 2 (Nrf2) and the heme oxygenase-1 (HO-1) were detected. The experiment revealed that EGCG treatment decreased HH-induced elevation of cardiac enzymes and relieved mitochondrial damage of the LV. Notably, EGCG treatment significantly alleviated oxidative stress in the LV and inflammatory response in the blood. Western blot confirmed that EGCG significantly upregulated Nrf2 and HO-1. Therefore, EGCG may be considered a promising natural compound for treating the HH-induced myocardial injuries.