Why the study?
Bawei Chenxiang powder is used for cardiovascular diseases, but the mechanisms underlying its protective effects against myocardial ischemia-reperfusion damage remained to be explored.
Does Bawei Chenxiang powder-containing serum improve survival and reduce oxidative stress in H9C2 cells subjected to hypoxia/reoxygenation?
Does Bawei Chenxiang powder-containing serum improve survival and reduce oxidative stress in H9C2 cells subjected to hypoxia/reoxygenation?
Bawei Chenxiang powder protects H9C2 cardiomyocytes from hypoxia/reoxygenation injury by reducing oxidative stress via the PI3K-AKT pathway.
Supports mechanistic study of BWCX in ischemia-reperfusion injury; leaves open clinical translation pending trials.
Ischemia-reperfusion damage to cardiomyocytes is one of the main directions of cardiovascular disease research, and Bawei Chenxiang powder (BWCX) is a traditional ethnomedicinal compound preparation mainly used in the treatment of cardiovascular diseases. On the basis of serum pharmacology, the present study aimed to explore the potential mechanism of BWCX against myocardial ischemia-reperfusion damage to cardiomyocytes. We prepared BWCX-serum containing. Using serum pharmacology and bioinformatics approaches, we explored its protective effects on H9C2 cells in a hypoxia/reoxygenation (H/R) model. Additionally, we investigated the underlying mechanisms. BWCX-containing serum can increase the survival rate of H9C2 cells and reduce oxidative stress levels in an H/R model. Specifically, it decreases the release of malondialdehyde (MDA), lactate dehydrogenase (LDH), creatine kinase (CK), and reactive oxygen species (ROS), while increasing the levels of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), and Complex I. Additionally, it downregulates the expression of NADH dehydrogenase (ubiquinone) 1 alpha sub-Complex 10 (NDUFA-10), thioredoxin (Trx), heme oxygenase 1 (HO-1), and kelch-like ECH-associated protein 1 (Keap1), and it upregulates the expression of nuclear factor erythroid 2-related factor 2 (Nrf2). These effects are potentially mediated through the PI3K-AKT pathway. In the present study, we found that BWCX powder exhibited significant ameliorative and reparative effects on H/R-induced cardiomyocyte injury by alleviating the level of oxidative stress during H/R and acting on the PI3K-AKT pathway.
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Gong et al. (2024) studied this question.
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