Journal of ethnopharmacology · 2025
Danggui Buxue decoction activates AMPK/PGC-1α pathway to improve chronic heart failure.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Qin Xiao-Jing, Gao Fan, Gao Sheng-Yun, Tian Jia-Ye, Liu Xing-Chao, Yang Ze-Qi, Guo Qiu-Hong
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Danggui Buxue Decoction (DBD) is a famous traditional Chinese medicine (TCM) formula. It has been shown to have cardiovascular benefits. In past studies, DBD has successfully improved the cardiac function of patients with chronic heart disease. However, the mechanism of DBD on myocardial injury in chronic heart failure (CHF)models remains unclear.
AIM: To investigate whether DBD can alleviate myocardial injury in CHF rats by improving abnormal myocardial energy metabolism.
MATERIALS AND METHODS: To ensure the quality of DBD preparations, we employed high-performance liquid chromatography (HPLC). A rat model of congestive heart failure (CHF) was created through surgical ligation of the transverse aortic arch. Sprague-Dawley (SD) rats were randomly assigned to six experimental groups: sham, model, trimetazidine (positive control), and three DBD treatment groups (high, medium, and low doses). Cardiac function was evaluated by echocardiography. The measurements include hemodynamics, cardiac injury records, oxidants and myocardial pathological changes. Transmission electron microscopy revealed ultrastructural changes in cardiac mitochondria. Detect the enzyme activities of mitochondrial respiratory chain complexes I, II, III, and IV and the activity of FAO. Levels of proteins associated with mitochondrial energy metabolic pathways in myocardial tissue (AMPK, p-AMPK, PGC-1α, CTP-1, GLUT4, NRF1, and mtTFA) are detected.
RESULTS: The preparation method of DBD by HPLC is feasible. DBD treatment improved cardiac function, inhibited myocardial injury and oxidative stress level induced by CHF. In addition, DBD can effectively improve myocardial mitochondrial structural damage, activities of respiratory chain enzymes I-IV, activity of FAO, activity abnormal glucose and lipid metabolism, and abnormal ATP expression level, and maintain the balance of energy metabolism in myocardial tissue. In addition, DBD alleviates myocardial injury in CHF rats by regulating AMPK/PGC-1α signaling pathway to improve abnormal energy metabolism of myocardial tissue.
CONCLUSIONS: DBD has the potential to counteract heart failure-induced cardiac impairment and preserve myocardial tissue integrity by modulating energy metabolism. This beneficial effect likely stems from DBD's ability to influence the AMPK/PGC-1α signaling pathway, which plays essential role in regulating cellular energy processes.
AIM: To investigate whether DBD can alleviate myocardial injury in CHF rats by improving abnormal myocardial energy metabolism.
MATERIALS AND METHODS: To ensure the quality of DBD preparations, we employed high-performance liquid chromatography (HPLC). A rat model of congestive heart failure (CHF) was created through surgical ligation of the transverse aortic arch. Sprague-Dawley (SD) rats were randomly assigned to six experimental groups: sham, model, trimetazidine (positive control), and three DBD treatment groups (high, medium, and low doses). Cardiac function was evaluated by echocardiography. The measurements include hemodynamics, cardiac injury records, oxidants and myocardial pathological changes. Transmission electron microscopy revealed ultrastructural changes in cardiac mitochondria. Detect the enzyme activities of mitochondrial respiratory chain complexes I, II, III, and IV and the activity of FAO. Levels of proteins associated with mitochondrial energy metabolic pathways in myocardial tissue (AMPK, p-AMPK, PGC-1α, CTP-1, GLUT4, NRF1, and mtTFA) are detected.
RESULTS: The preparation method of DBD by HPLC is feasible. DBD treatment improved cardiac function, inhibited myocardial injury and oxidative stress level induced by CHF. In addition, DBD can effectively improve myocardial mitochondrial structural damage, activities of respiratory chain enzymes I-IV, activity of FAO, activity abnormal glucose and lipid metabolism, and abnormal ATP expression level, and maintain the balance of energy metabolism in myocardial tissue. In addition, DBD alleviates myocardial injury in CHF rats by regulating AMPK/PGC-1α signaling pathway to improve abnormal energy metabolism of myocardial tissue.
CONCLUSIONS: DBD has the potential to counteract heart failure-induced cardiac impairment and preserve myocardial tissue integrity by modulating energy metabolism. This beneficial effect likely stems from DBD's ability to influence the AMPK/PGC-1α signaling pathway, which plays essential role in regulating cellular energy processes.