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Bergenin alleviates myocardial ischemia-reperfusion injury via SIRT1 signaling
Yingying Liu1, Yanzhen Tan2, Guojie Cao3
1College of Life Science, Northwest University, Xi'an 710069, China; Department of Cardiovascular Surgery, Xijing Hospital, Fourth Military Medical University, Xi'an 710032, China.
Abstract:
Myocardial ischemia-reperfusion (MI/R) is a major risk factor for cardiovascular disease. At present, reducing oxidative stress and apoptosis is a crucial therapeutic strategy for ameliorating MI/R injury. However, there is a lack of drugs targeting oxidative stress and apoptosis for the clinical therapy of MI/R. Bergenin is a reportedly effective agent with antioxidative and antiapoptotic activity against acute injury. Nevertheless, the roles and potential mechanisms of bergenin against MI/R injury remain unknown. Here, we hypothesized that bergenin attenuated MI/R-induced apoptosis and reactive oxygen species (ROS) production via SIRT1. Mice were subjected to MI/R and treated with bergenin, after which the cardiac function, cardiomyocyte apoptosis, LDH release, and MDA content were evaluated. In vitro, myocardial injury model of H9c2 cells was induced by simulated ischemia/reperfusion (SI/R), apoptosis and oxidative stress was decreased after treated with bergenin. Bergenin significantly reduced myocardial apoptosis and ROS generation in vitro and improved cardiac function in vivo. Intriguingly, bergenin remarkably decreased apoptosis in cardiac tissue accompanied by SIRT1 upregulation following MI/R injury. Further studies showed that inhibiting SIRT1 blocked bergenin's beneficial impact against apoptosis following SI/R injury through excessive oxidative stress and depression of the Bcl2 to Bax ratio. Collectively, these findings indicate that bergenin alleviates MI/R injury by ameliorating myocardial apoptosis and oxidative damage via the SIRT1 signaling pathway.
Insights
Bergenin protects against heart injury from ischemia-reperfusion (MI/R) by reducing oxidative stress and apoptosis. This protection is mediated through the SIRT1 signaling pathway, offering a potential therapeutic strategy for cardiovascular disease.
Area of Science:
- Cardiovascular Science
- Molecular Biology
- Pharmacology
Background:
- Myocardial ischemia-reperfusion (MI/R) injury is a significant contributor to cardiovascular disease.
- Current therapeutic strategies focus on reducing oxidative stress and apoptosis, but effective drugs are limited.
- Bergenin shows potential antioxidative and antiapoptotic properties, yet its mechanism in MI/R injury is unexplored.
Purpose of the Study:
- To investigate the protective effects and underlying mechanisms of bergenin against MI/R injury.
- To determine if bergenin's effects involve the SIRT1 signaling pathway.
- To evaluate bergenin's impact on cardiac function, apoptosis, and oxidative stress in MI/R models.
Main Methods:
- In vivo studies involved inducing MI/R in mice treated with bergenin, assessing cardiac function, apoptosis, LDH, and MDA levels.
- In vitro studies utilized a simulated ischemia/reperfusion (SI/R) model in H9c2 cells treated with bergenin.
- Investigated the role of SIRT1 by using inhibitors and examining its expression and downstream targets (Bcl2/Bax ratio).
Main Results:
- Bergenin treatment improved cardiac function and reduced cardiomyocyte apoptosis, LDH release, and MDA content in vivo.
- In vitro, bergenin decreased apoptosis and oxidative stress in SI/R-induced H9c2 cells.
- Bergenin upregulated SIRT1 expression in cardiac tissue post-MI/R, and SIRT1 inhibition abolished bergenin's protective effects.
Conclusions:
- Bergenin effectively alleviates MI/R injury by reducing myocardial apoptosis and oxidative damage.
- The protective mechanism of bergenin is significantly mediated through the activation of the SIRT1 signaling pathway.
- Bergenin represents a promising therapeutic agent for managing MI/R-induced cardiovascular damage.
