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The present study aimed to investigate the cardioprotective effects of acteoside (AC) on myocardial ischemia‑reperfusion injury (MIRI). To meet this aim, a network pharmacological analysis was conducted to search for key genes and signaling pathways associated with AC and MIRI. The infarct size of the rat heart was evaluated using 2,3,5‑triphenyltetrazolium chloride staining, and the serum levels of creatine kinase MB isoenzyme, cardiac troponin I, malondialdehyde and superoxide dismutase were subsequently detected in an experiment.

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Background: Myocardial ischemia-reperfusion injury (MIRI) is an important complication in the treatment of heart failure, and its treatment has not made satisfactory progress. Nitroxyl (HNO) showed protective effects on the heart failure, however, the effect and underlying mechanism of HNO on MIRI remain largely unclear.

Methods: MIRI model in this study was established to induce H9C2 cell injury through hypoxia/reoxygenation (H/R) in vitro.

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Cardiac Positron Emission Tomography (PET) can be used for the assessment of myocardial perfusion. Compared to other cardiac imaging techniques, notably Single Photon Emission Computer Tomography (SPECT), cardiac PET offers superior image resolution, higher accuracy, quantitative measures of myocardial perfusion, lower radiation exposure, and shorter image acquisition time. However, PET tends to be costlier and less widely available than SPECT due to the specialized equipment needed for generating the necessary radiotracers.

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Cannabidiol Ameliorates Doxorubicin-Induced Myocardial Injury via Activating Hippo Pathway.

Drug Des Devel Ther

January 2025

School of Basic Medicine, Jiamusi University, Jiamusi, Heilongjiang, 154000, People's Republic of China.

Background: Doxorubicin (DOX) is a chemotherapeutic agent widely used for cancer treatment and has non-negligible cardiotoxicity. Some previous studies have reported that cannabidiol (CBD) has cardioprotective effects. In this study, we evaluated the protective effects of CBD against DOX-induced cardiomyocyte injury, and explored the downstream molecular mechanism.

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Purpose: This study aims to investigate whether zinc ion (Zn) alleviates myocardial ischemia-reperfusion injury (MIRI) through the MAM-associated signaling pathway and to explore its impact on ERS and calcium overload.

Methods: H9C2 cells were cultured in a DMEM supplemented with 10 % fetal bovine serum and 1 % antibiotic solution. A MIRI model was established through simulated ischemia and reoxygenation with Zn treatment in a complete medium.

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