Shen Qi Li Xin formula improves chronic heart failure through balancing mitochondrial fission and fusion via upregulation of PGC-1α
| العنوان: | Shen Qi Li Xin formula improves chronic heart failure through balancing mitochondrial fission and fusion via upregulation of PGC-1α |
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| المؤلفون: | Yan-Bo Sui, Bi-Hong Sun, Pei-Pei Pan, Li Liu, Jin-Xuan Wei, Jian Xiu |
| المصدر: | The Journal of Physiological Sciences. 71 |
| بيانات النشر: | Springer Science and Business Media LLC, 2021. |
| سنة النشر: | 2021 |
| مصطلحات موضوعية: | Heart Failure, Membrane Potential, Mitochondrial, Cardiac function curve, TUNEL assay, Physiology, Chemistry, Apoptosis, Pharmacology, medicine.disease, medicine.disease_cause, Mitochondrial Dynamics, Rats, Up-Regulation, mitochondrial fusion, Heart failure, medicine, Animals, Humans, Myocytes, Cardiac, Mitochondrial fission, Viability assay, Oxidative stress |
| الوصف: | 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. |
| تدمد: | 1880-6562 1880-6546 |
| URL الوصول: | https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d86dfa100fb497c02219da3f7213d351 https://doi.org/10.1186/s12576-021-00816-y |
| حقوق: | OPEN |
| رقم الأكسشن: | edsair.doi.dedup.....d86dfa100fb497c02219da3f7213d351 |
| قاعدة البيانات: | OpenAIRE |
Find this article in full text from Springer Verlag. | تدمد: | 18806562 18806546 |
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