Protective effect of glycyrrhizin on coronary microembolization-induced myocardial dysfunction in rats
Yonggang Yuan1, Bing Li1, Wanzhong Peng1
1Department of Cardiology, Cangzhou Central Hospital of Tianjin Medical University, Hebei, China.
Insights
Glycyrrhizin, a High-Mobility Group Box-1 (HMGB1) inhibitor, protects against coronary microembolization (CME)-induced heart dysfunction. It reduces inflammation and cardiomyocyte apoptosis by inhibiting the HMGB1/TLR4/NF-κB pathway.
Area of Science:
- Cardiology
- Pharmacology
- Molecular Biology
Background:
- Coronary microembolization (CME) causes myocardial dysfunction through inflammation and cardiomyocyte apoptosis.
- High-mobility group box-1 (HMGB1) is crucial in CME progression, and its inhibition offers protection.
Purpose of the Study:
- To evaluate the protective effects of glycyrrhizin, a HMGB1 inhibitor, against CME-induced myocardial dysfunction in a rat model.
Main Methods:
- Rats were treated with glycyrrhizin before CME induction.
- Measurements included HMGB1, inflammatory cytokines (TNF-α, iNOS, IL-6, IL-1β), apoptosis markers (cleaved caspase-3, Bax, Bcl-2), cardiac enzymes (troponin I, creatine kinase), cardiac function, and TLR4/NF-κB pathway activation.
Main Results:
- Glycyrrhizin reduced HMGB1, inflammatory cytokines, and cardiomyocyte apoptosis.
- It decreased cardiac troponin I and creatine kinase levels, improving cardiac function.
- Glycyrrhizin inhibited the HMGB1/TLR4/NF-κB signaling pathway.
Conclusions:
- Glycyrrhizin ameliorates myocardial dysfunction in CME rats.
- This protection is achieved by preventing inflammation and cardiomyocyte apoptosis via HMGB1/TLR4/NF-κB pathway inhibition.
Abstract:
Coronary microembolization (CME)-induced inflammation and cardiomyocyte apoptosis are two key factors contributing to CME-induced myocardial dysfunction. High-mobility group box-1 (HMGB1) plays essential role in progression of CME-induced injury and inhibition of HMGB1 has been shown to be protective. In present study, the potential effects of glycyrrhizin, a HMGB1 inhibitor, on CME-induced myocardial dysfunction are evaluated. Using a rat model of CME, we administrated glycyrrhizin in rats prior to CME induction. The level of HMGB1, TNF-α, iNOS, IL-6, IL-1β, cleaved caspase-3, Bax, and Bcl-2 were measured. The serum level of cardiac troponin I, creatine kinase, was detected. The cardiac function and cardiomyocyte apoptosis were evaluated. The activation of TLR4/NF-κB signaling pathway was analyzed. Glycyrrhizin prevented CME-induced production of HMGB1, TNF-α, iNOS, IL-6, and IL-1β. Glycyrrhizin inhibited CME-induced cardiomyocyte apoptosis and the expression of cleaved caspase-3 and Bax, while enhanced the expression of Bcl-2. Glycyrrhizin decreased cardiac troponin I and creatine kinase levels and improved cardiac function. Glycyrrhizin prevented the activation of HMGB1/TLR4/NF-κB signaling pathway. Glycyrrhizin ameliorated myocardial dysfunction in CME rats by preventing inflammation and apoptosis of cardiomyocytes.
