During
myocardial infarction, quickly opening the occluded coronary artery is a major method to save the ischemic myocardium. However, it also induces
reperfusion injury, resulting in a poor prognosis. Alleviating the
reperfusion injury improves the prognosis of the patients.
Dihydromyricetin (DHM), a major component in the Ampelopsis grossedentata, has numerous biological functions. This study aims to clarify the effects of DHM under the
ischemia/reperfusion (I/R) condition. We elucidated the role of
Sirt3 in the cardiomyocyte response to DHM based on the hearts and primary cardiomyocytes. Cardiac function, mitochondrial biogenesis, and
infarct areas were examined in the different groups. We performed Western blotting to detect
protein expression levels
after treatments. In an in vitro study, primary cardiomyocytes were treated with
Hypoxia/Reoxygenation (H/R) to simulate the I/R. DHM reduced the
infarct area and improved cardiac function. Furthermore,
mitochondrial dysfunction was alleviated after DHM treatment. Moreover, DHM alleviated oxidative stress indicated by decreased ROS and MnSOD. However, the beneficial function of DHM was abolished after removing the
Sirt3. On the other hand, the mitochondrial function was improved after DHM intervention in vitro study. Interestingly,
Sirt3 downregulation inhibited the beneficial function of DHM. Therefore, the advantages of DHM are involved in the improvement of mitochondrial function and decreased oxidative stress through the upregulation of
Sirt3. DHM offers a promising therapeutic avenue for better outcome in the patients with cardiac I/R injury.