Key result
Poge heart-saving decoction improves cardiac function and attenuates myocardial fibrosis in mice via PI3K/AKT inhibition.
Why the study?
Poge Heart-Saving Decoction has been used clinically for decades to treat heart failure, but its precise therapeutic mechanisms remain incompletely understood.
Does Poge Heart-Saving Decoction ameliorate heart failure by suppressing apoptosis and fibrosis in a mouse model?
Does Poge Heart-Saving Decoction ameliorate heart failure by suppressing apoptosis and fibrosis in a mouse model?
p-value: p=<0.05
Poge Heart-Saving Decoction improves cardiac function and attenuates myocardial apoptosis and fibrosis in a mouse model of heart failure by inhibiting the PI3K/AKT pathway.
Hypothesis-generating for Poge heart-saving decoction in HF; prospective trials needed before clinical adoption.
Background Poge Heart-Saving Decoction (PHSD) is a traditional Chinese medicine formulation that has been used clinically for decades in the treatment of heart failure (HF). However, its precise therapeutic mechanisms remain incompletely understood. Methods The metabolites of PHSD were characterized using UHPLC-MS/MS. Network analysis was subsequently employed to identify the mechanism. A mouse model of HF was established through intraperitoneal injection of isoproterenol (ISO), followed by treatment with PHSD at low, medium or high doses. Cardiac function parameters were evaluated by echocardiography, and NT-proBNP levels were measured. Histopathological examination of myocardial tissue was conducted, complemented by analyses of protein and mRNA expression levels related to apoptosis and fibrosis targeting the PI3K/AKT pathway. Results A total of 133 metabolites in PHSD were identified. Network analysis suggested that PHSD may ameliorate HF by targeting key proteins such as AKT1, TNF, and BCL-2. In vivo experiments demonstrated that PHSD alleviated ISO-induced myocardial apoptosis by balanced BAX and BCL-2. Furthermore, PHSD significantly reduced the deposition of Collagen I and Collagen III and markedly downregulated the expression of PI3K and AKT. Conclusion Our study demonstrated that PHSD ameliorates HF by suppressing myocardial apoptosis and fibrosis through inhibition of the PI3K/AKT pathway. These findings indicate that PHSD is a prospective therapeutic agent against HF.
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Du et al. (2026) studied Heart failure (n=60). Poge heart-saving decoction (PHSD) vs. Isoproterenol (model) and Deslanoside was evaluated on Cardiac function (EF, FS, LVIDs, LVIDd) and myocardial apoptosis/fibrosis (p=<0.05). Poge heart-saving decoction significantly improved cardiac function and attenuated isoproterenol-induced myocardial apoptosis and fibrosis in mice by inhibiting the PI3K/AKT signaling pathway.
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