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Schisandrin a Ameliorates Cardiac Injury and Dysfunction Induced by Hemorrhagic Shock via Activating the Nrf2
Bo Li1, Wuming Zhou2, Jiacheng Zhang2
1Department of Pharmacy, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, Liaoning 121000, P. R. China.
Insights
Schisandrin A protects the heart from damage caused by hemorrhagic shock (HS). It reduces cell death, oxidative stress, and mitochondrial dysfunction by activating the Nrf2 pathway.
Area of Science:
- Cardiovascular Biology
- Pharmacology
- Cellular Physiology
Background:
- Hemorrhagic shock (HS) leads to significant cardiac injury and dysfunction, contributing to high mortality.
- Schisandrin A (Sch A), a natural compound, has known anti-inflammatory and antioxidant properties.
- The protective effects of Sch A on HS-induced cardiac injury remain largely unexplored.
Purpose of the Study:
- To investigate the therapeutic potential of Schisandrin A (Sch A) in mitigating cardiac injury and dysfunction following hemorrhagic shock (HS).
- To elucidate the underlying molecular mechanisms, including apoptosis, oxidative stress, mitochondrial function, and Nrf2 signaling, involved in Sch A's protective effects.
Main Methods:
- Hemorrhagic shock (HS) rat model established via femoral artery blood withdrawal, followed by fluid resuscitation.
- Assessment of cardiac function and pathological changes.
- Evaluation of apoptosis markers (cleaved-caspase-3, -9), reactive oxygen species (ROS) levels, oxidative stress indicators, mitochondrial membrane potential (MMP), and cytochrome c (Cyto c) transformation.
- Analysis of Nrf2 signaling pathway activation.
Main Results:
- HS induced significant cardiac dysfunction and pathological injury, which were dose-dependently attenuated by Sch A.
- Sch A suppressed HS-induced apoptosis by reducing cleaved-caspase-3 and -9 expression.
- Sch A mitigated excessive ROS production, improved oxidative stress markers, and restored mitochondrial function (MMP, Cyto c release).
- The protective effects of Sch A were mediated by the activation of the Nrf2 signaling pathway.
Conclusions:
- Schisandrin A (Sch A) effectively ameliorates cardiac injury and dysfunction induced by hemorrhagic shock (HS).
- Sch A exerts its protective effects by suppressing apoptosis, reducing oxidative stress, and improving mitochondrial function.
- Activation of the Nrf2 signaling pathway is a key mechanism underlying Sch A's cardioprotective action in HS.
Abstract:
Hemorrhagic shock (HS) is a critical condition with high mortality caused by acute blood loss. Cardiac injury and dysfunction induced by HS is a major factor associated with the poor prognosis of affected patients. Schisandrin A (Sch A), a dibenzocyclooctadiene lignan extracted from Fructus schisandrae, exhibits multiple biological activities, including anti-inflammatory, and antioxidant effects. However, the effect of Sch A on HS-caused cardiac injury and its underlying mechanism still lack research. In this study, we established an HS rat model through blood loss from the femoral artery and monitoring mean arterial pressure (MAP) followed by fluid resuscitation. Our findings suggested that cardiac dysfunction and pathological injury were induced by HS and attenuated by Sch A treatment in a dose-dependent manner. Apoptosis in cardiac tissue was promoted by HS, but suppressed after administration of Sch A by decreasing the protein expressions of cleaved-caspase-3 and -9. Moreover, excessive ROS production induced by HS was mitigated by Sch A, and the levels of oxidative stress indicators were improved by Sch A. Additionally, HS triggered the reduction of mitochondrial membrane potential (MMP), and led to mitochondrial dysfunction. Sch A reversed this effect of HS on mitochondria. The transformation of cytochrome c (Cyto c) induced by HS was also restored by Sch A. Importantly, the activation of the Nrf2 signaling pathway mediated the protective effects of Sch A against cardiac injury induced by HS. In conclusion, it was found that Sch A ameliorated HS-induced cardiac injury and dysfunction through suppressing apoptosis and oxidative stress, as well as alleviating mitochondrial dysfunction via the Nrf2 signaling pathway.
