Resveratrol alleviates alveolar epithelial cell injury induced by hyperoxia by reducing apoptosis and mitochondrial
Xiaodan Zhu1,2,3, Fan Wang1,2,3, Xiaoping Lei1,2,3
1Division of Neonatology, Department of Pediatrics, The Affiliated Hospital of Southwest Medical University, Luzhou 646000, China.
Insights
Resveratrol protects premature infants from bronchopulmonary dysplasia by improving mitochondrial function and reducing cell death. This natural compound activates Sirtuin 1, offering a potential therapeutic pathway for lung injury.
Area of Science:
- Cell Biology
- Molecular Medicine
- Neonatal Research
Background:
- Bronchopulmonary dysplasia (BPD) is a chronic lung disease in premature infants, significantly influenced by hyperoxia-induced acute lung injury.
- Resveratrol, a natural polyphenol, is known to activate Sirtuin 1 (SIRT1) and shows promise in mitigating lung damage, but its precise protective mechanisms remain unclear.
Purpose of the Study:
- To elucidate the protective mechanisms of resveratrol against hyperoxia-induced lung injury in human alveolar epithelial cells.
- To investigate the role of the SIRT1/PGC-1α signaling pathway in resveratrol's protective effects.
Main Methods:
- A cell model of hyperoxia-induced acute lung injury was established using human alveolar epithelial cells.
- Cells were treated with resveratrol (Res), the SIRT1 activator SRT1720, and the SIRT1 inhibitor EX-527 under hyperoxic conditions.
- Mitochondrial function, apoptosis, and the expression of key proteins (SIRT1, PGC-1α, NRF1, TFAM, acetyl-p53) were analyzed.
Main Results:
- Resveratrol and SRT1720 significantly alleviated hyperoxia-induced apoptosis and mitochondrial dysfunction.
- Both resveratrol and SRT1720 upregulated SIRT1, PGC-1α, NRF1, and TFAM expression.
- Acetyl-p53 levels were decreased by resveratrol and SRT1720 treatment under hyperoxia.
Conclusions:
- Resveratrol protects alveolar epithelial cells from hyperoxia-induced injury by enhancing mitochondrial function and reducing apoptosis.
- The protective effects are mediated through the SIRT1/PGC-1α signaling pathway, highlighting SIRT1 upregulation as a key factor in lung protection.
Abstract:
Bronchopulmonary dysplasia is a severe and long-term pulmonary disease in premature infants. Hyperoxia-induced acute lung injury plays a critical role in bronchopulmonary dysplasia. Resveratrol is a polyphenolic phytoalexin and a natural agonist of Sirtuin 1. Many studies have shown that resveratrol has a protective effect on hyperoxia-induced lung damage, but its specific protective mechanism is still not clear. Further exploration of the possible protective mechanism of resveratrol was the main goal of this study. In this study, human alveolar epithelial cells were used to establish a hyperoxia-induced acute lung injury cell model, and resveratrol (Res or R), the Sirtuin 1 activator SRT1720 (S) and the Sirtuin 1 inhibitor EX-527 (E) were administered to alveolar epithelial cells, which were then exposed to hyperoxia to investigate the role of Res in mitochondrial function and apoptosis. We divided human alveolar epithelial cells into the following groups: (1) the control group, (2) hyperoxia group, (3) hyperoxia+Res20 group, (4) hyperoxia+Res20+E5 group, (5) hyperoxia+Res20+E10 group, (6) hyperoxia+S2 group, (7) hyperoxia+S2+E5 group, and (8) hyperoxia+S2+E10 group. Hyperoxia-induced cell apoptosis and mitochondrial dysfunction were alleviated by Res and SRT1720. Res and SRT1720 upregulated Sirtuin 1, PGC-1α, NRF1, and TFAM but decreased the expression of acetyl-p53 in human alveolar epithelial cells that were exposed to hyperoxia. These findings revealed that Res may alleviated hyperoxia-induced mitochondrial dysfunction and apoptosis in alveolar epithelial cells through the SIRT1/PGC-1a signaling pathway. Thus, Sirtuin 1 upregulation plays an important role in lung protection.
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