AI Article Synopsis
- SQLXF has been shown to improve heart function in chronic heart failure patients, but its mechanism is not fully understood.
- In studies, SQLXF reduced signs of myocardial damage and improved heart parameters in CHF rats, while also promoting beneficial mitochondrial protein expressions.
- The formula works by inhibiting apoptosis in heart cells and reducing oxidative stress, suggesting a new mechanism for its effectiveness in treating heart failure.
Article Abstract
Background: Our previous study proved that Shen Qi Li Xin formula (SQLXF) improved the heart function of chronic heart failure (CHF) patients, while the action mechanism remains unclear.
Methods: H&E staining and TUNEL staining were performed to measure myocardial damages. Western blot was used to examine the expression of proteins. Moreover, CCK-8 assay and flow cytometry were used to measure cell viability and cell apoptosis, respectively. Concentrations of ATP and ROS in cells, and mitochondrial membrane potential (MMP) were detected to estimate oxidative stress.
Results: In vivo, we found that SQLXF improved cardiac hemodynamic parameters, reduced LDH, CK-MB and BNP production, and attenuated myocardial damages in CHF rats. Besides, SQLXF promoted mitochondrial fusion-related proteins expression and inhibited fission-related proteins expression in CHF rats and oxygen glucose deprivation/reoxygenation (OGD/R)-induced cardiac myocytes (CMs). In vitro, our data show that certain dose of SQLXF inhibited OGD/R-induced CMs apoptosis, cell viability decreasing and oxidative stress.
Conclusion: Overall, certain dose of SQLXF could effectively improve the cardiac function of CHF rats through inhibition of CMs apoptosis via balancing mitochondrial fission and fusion. Our data proved a novel action mechanism of SQLXF in CHF improvement, and provided a reference for clinical.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10717454 | PMC |
| http://dx.doi.org/10.1186/s12576-021-00816-y | DOI Listing |
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