Key result
Liguzinediol improves ejection fraction by ~14% versus vehicle in rats with post-MI heart failure.
Why the study?
Current clinical drugs used to treat heart failure may cause serious side effects, prompting evaluation of the novel compound liguzinediol.
Does liguzinediol improve cardiac function and attenuate ventricular remodeling in a rat model of heart failure induced by myocardial infarction?
Does liguzinediol improve cardiac function and attenuate ventricular remodeling in a rat model of heart failure induced by myocardial infarction?
Liguzinediol improves cardiac function and attenuates ventricular remodeling in a rat model of post-myocardial infarction heart failure, potentially through the regulation of the TGF-β1/Smads pathway.
Background Heart failure (HF) is one of the most common causes of cardiovascular diseases in the world. Currently, the drugs used to treat HF in the clinic may cause serious side effects. Liguzinediol, 2, 5-dimethyl-3, 6-dimethyl-pyrazine, is a compound synthesized after the structural modification of ligustrazine (one active ingredient of Szechwan Lovage Rhizome ). We aimed to observe the effects of liguzinediol on preventing HF and explore the related mechanisms. Methods The ligation of left anterior descending coronary artery was operated to established the myocardial infarction (MI) model in Sprague–Dawley rats. Cardiac functions were recorded by echocardiography and hemodynamics. The changes in the Renin–Angiotensin–Aldosterone System (RAAS), inflammation, and oxidative stress were detected by radioimmunoassay and Elisa kits. Western blot and real-time PCR were applied to determine the expressions of the TGF-β1/Smads pathway. Results Firstly, liguzinediol enhanced the systolic and diastolic functions of the heart in MI rats. Liguzinediol improved ventricular remodeling by reducing myocardial cell necrosis, as well as reducing collagen deposition and myocardial fibrosis. Then, liguzinediol suppressed the activation of RAAS, inhibited the synthesis of pro-inflammation factors, and reduced oxidative stress. In the end, liguzinediol also down-regulated the expressions of the TGF-β1/Smads pathway. Conclusions Liguzinediol could alleviate HF caused by MI in rats, and the protective effect was associated with the regulation of the TGF-β1/Smads pathway.
No takes yet. Share an insight, caveat, or question.
Chen et al. (2020) studied Heart failure induced by myocardial infarction (n=80). Liguzinediol vs. Vehicle (MI group), Captopril (10 mg/kg), Digoxin (0.032 mg/kg) was evaluated on Ejection fraction (EF) at 8 weeks (p=<0.01). Liguzinediol (20 mg/kg) significantly improved ejection fraction to 54.34% compared to 40.41% in vehicle-treated rats with myocardial infarction-induced heart failure.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: