The protective effects of liguzinediol on congestive heart failure induced by myocardial infarction and its relative mechanism

Abstract

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-dimethylpyrazine, 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.

Ligustrazine and liguzinediol protect against doxorubicin‐induced cardiomyocytes injury by inhibiting mitochondrial apoptosis and autophagy

“…Our previous study revealed that liguzinediol has a high therapeutic effect on HF, and it could improve myocardial cell apoptosis in stress-induced HF. [24][25][26] However, it is still unknown whether liguzinediol can improve HF caused by promoting autophagy in salvaged cardiomyocytes. In this study, we aimed to establish a model of HF caused by doxorubicin (DOX) and to investigate the protective effect of liguzinediol.…”

Sulforaphane Effects on Cardiac Function and Calcium-Handling–Related Proteins in 2 Experimental Models of Heart Disease: Ischemia-Reperfusion and Infarction

“…These alterations in cardiac morphology and function were expected as a consequence of MI and were also described in previous studies. 30,48–50 However, none of the echocardiographic parameters were improved after SFN administration. Similar results were found in a study from our group that evaluated SFN effects after infarction, 28 days after the surgery.…”

The Therapeutic Effects of Ligustrazine in Combination with Other Drugs in Cardiovascular Diseases

“…In addition to cardiac protection, paeoniflorin (Shao Yao Dai) inhibits tert-butyl hydroperoxide-induced mitochondrial reactive oxygen species (ROS) production in human umbilical vein endothelial cells (HUVECs) and ROS-mediated proliferation of vascular smooth muscle cells, indicating a potential therapeutic effect on diseases related to abnormal vascular remodeling [34,35]. Ligustrazine (Chuan Xiong Qin) improved cardiac function accompanied by decreased cell necrosis, collagen deposition, myocardial fibrosis, expression of pro-inflammatory factors, and oxidative stress in the Sprague-Dawley (SD) rats with myocardial infarction [36]. Ligustrazine (Chuan Xiong Qin) and paeoniflorin (Shao Yao Dai) are both the main components of ligusticum chuanxiong Hort, and they have a similar protective effect on cardiac injury.…”