Journal of ethnopharmacology · 2026
Shenqi Oral Liquid regulates reactive oxygen species production by modulating autophagy, thereby regulating mitochondrial dynamics in cardiomyocytes and alleviating chronic heart failure in mice via adenosine 5'-monophosphate-activated protein kinase/mechanistic target of rapamycin axis.
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Xie Xueqing, Ge Hongyao, Hu Xianrun, Gao Xuan, Song Yingying, Xie Longfei, Wu Hui, Huang Fei, Wang Changhong, Shi Hailian, Wu Xiaojun
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Shenqi Oral Liquid (SOL) originated from the "Discerning Internal and External Injuries" is a Chinese formula composed of two herbs: Codonopsis pilosula (Franch.) Nannf. (Dang-shen) and Astragalus membranaceus (Fisch.) Bunge. (Huang-qi). This formula has been used clinically for many years to treat chronic heart failure (CHF). However, the specific mechanism of SOL in treating CHF is still unclear.
AIM OF THE STUDY: The aim of this study was to evaluate the protective effect of SOL on the decline in cardiac function in doxorubicin (DOX)-induced CHF mice and to explore the potential molecular mechanisms.
MATERIALS AND METHODS: A CHF mouse model was established by administering 5 mg/kg/week DOX via intraperitoneal injection for 6 consecutive weeks. Then, CHF model mice were treated with low-dose (0.6 g/kg) and high-dose (1.2 g/kg) SOL via oral gavage for 4 consecutive weeks. Therapeutic effects of SOL on heart failure were evaluated using cardiac ultrasound, electrocardiography, biochemical index, and histological staining. Network pharmacology and transcriptomics were employed to identify potential molecular mechanisms. Autophagy and mitochondrial dynamics were assessed using transmission electron microscope (TEM), dihydroethidium (DHE) staining, quantitative polymerase chain reaction (qPCR), western blotting (WB), and other methods. SOL-medicated serum and Rapamycin (Rapm) were applied to H9c2 cells to assess adenosine triphosphate (ATP) levels, autophagy occurrence, autophagy proteins, intracellular reactive oxygen species (ROS) levels, mitochondrial ROS levels, and mitochondrial membrane potential.
RESULTS: SOL significantly alleviated the decline of cardiac function in CHF mice, with the high-dose group showing the most pronounced effect. Network pharmacology and transcriptomics analysis indicated that SOL relieved CHF via modulation of autophagy, mitochondrial function, redox processes and apoptosis in cardiomyocytes. Further validation experiments indicated that SOL inhibited excessive autophagy by restraining the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) and adenosine 5'-monophosphate-activated protein kinase (AMPK) pathways in cardiomyocytes. Additional in vitro and in vivo experiments demonstrated that SOL rescued mitochondrial dysfunction and apoptosis in cardiomyocytes through inhibiting excessive autophagy.
CONCLUSIONS: SOL modulates myocardial mitochondrial dynamics by regulating ROS production through autophagy via the AMPK/mTOR axis, mitigating DOX-induced myocardial injury and alleviating CHF in mice.
AIM OF THE STUDY: The aim of this study was to evaluate the protective effect of SOL on the decline in cardiac function in doxorubicin (DOX)-induced CHF mice and to explore the potential molecular mechanisms.
MATERIALS AND METHODS: A CHF mouse model was established by administering 5 mg/kg/week DOX via intraperitoneal injection for 6 consecutive weeks. Then, CHF model mice were treated with low-dose (0.6 g/kg) and high-dose (1.2 g/kg) SOL via oral gavage for 4 consecutive weeks. Therapeutic effects of SOL on heart failure were evaluated using cardiac ultrasound, electrocardiography, biochemical index, and histological staining. Network pharmacology and transcriptomics were employed to identify potential molecular mechanisms. Autophagy and mitochondrial dynamics were assessed using transmission electron microscope (TEM), dihydroethidium (DHE) staining, quantitative polymerase chain reaction (qPCR), western blotting (WB), and other methods. SOL-medicated serum and Rapamycin (Rapm) were applied to H9c2 cells to assess adenosine triphosphate (ATP) levels, autophagy occurrence, autophagy proteins, intracellular reactive oxygen species (ROS) levels, mitochondrial ROS levels, and mitochondrial membrane potential.
RESULTS: SOL significantly alleviated the decline of cardiac function in CHF mice, with the high-dose group showing the most pronounced effect. Network pharmacology and transcriptomics analysis indicated that SOL relieved CHF via modulation of autophagy, mitochondrial function, redox processes and apoptosis in cardiomyocytes. Further validation experiments indicated that SOL inhibited excessive autophagy by restraining the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin (mTOR) and adenosine 5'-monophosphate-activated protein kinase (AMPK) pathways in cardiomyocytes. Additional in vitro and in vivo experiments demonstrated that SOL rescued mitochondrial dysfunction and apoptosis in cardiomyocytes through inhibiting excessive autophagy.
CONCLUSIONS: SOL modulates myocardial mitochondrial dynamics by regulating ROS production through autophagy via the AMPK/mTOR axis, mitigating DOX-induced myocardial injury and alleviating CHF in mice.