Key result
Panax notoginseng improves cardiac function and reduces myocardial fibrosis in preclinical heart failure.
Why the study?
The mechanism of Panax notoginseng in the treatment of heart failure was not fully understood and required exploration through network pharmacology and experimental verification.
Does Panax notoginseng improve cardiac function and reduce myocardial fibrosis in a post-MI heart failure rat model?
Does Panax notoginseng improve cardiac function and reduce myocardial fibrosis in a post-MI heart failure rat model?
Panax notoginseng improves cardiac function and attenuates myocardial fibrosis in a post-MI heart failure rat model, likely by regulating the p-p38 MAPK-TGF-β pathway.
Answers are grounded in this paper and cite their sources.
PNS mechanisms in rat post-MI HF models are hypothesis-generating; human trials needed before any clinical consideration.
Objective: This study aimed to explore the mechanism of Panax notoginseng (PNS) in the treatment of heart failure (HF) based on network pharmacology analysis combined with experimental verification. Materials and Methods: The potential targets and key pathways of effective components of PNS in the treatment of HF were revealed using network pharmacology. The postacute myocardial infarction (MI) HF rat model was established by ligating the left anterior descending branch of the coronary artery. The rats were divided into three groups: model, PNS, and fenofibrate groups. PNS (0.75 g/kg) and fenofibrate (10 mg/kg) were administered for 28 days. The efficacy and target mechanism of PNS in the treatment of HF were verified by cardiac ultrasound, Masson staining, and western blotting (WB) techniques. Results: The results of network pharmacology showed that seven potentially active compounds, such as quercetin, were obtained, involving 105 targets of HF; GO function was enriched to 1240 items; and KEGG enrichment covered 1240 signal pathways. The results of echocardiography showed that EF and FS of HF rats after MI were significantly increased, while Left ventricular internal dimension diastole (LVIDd) and Left ventricular internal dimension systole (LVIDs) were significantly decreased ( P < 0.001, P < 0.05). Masson staining showed that PNS could reduce the degree of myocardial fibrosis (MF) in HF. The results of WB showed that PNS could reduce the expression of the p-p38-MAPK, transforming growth factor-beta (TGF-β), and Smad3 in HF rats. Conclusion: PNS inhibited MF and treated HF by regulating p-p38 MAPK-TGF-β pathway, which lays a theoretical foundation for further study of its pharmacological mechanism and key target.
No takes yet. Share an insight, caveat, or question.
Peng et al. (2021) studied Heart failure. Panax notoginseng (PNS) vs. Model group and fenofibrate group was evaluated on Echocardiographic parameters (EF, FS, LVIDd, LVIDs), myocardial fibrosis, and protein expression (p=P < 0.001, P < 0.05). Panax notoginseng increased EF and FS and decreased LVIDd and LVIDs in heart failure rats, while reducing myocardial fibrosis via the p-p38 MAPK-TGF-β pathway.
Synapse has enriched 10 related papers. Consider them for comparative context: