Liquiritin Protects Against Cardiac Fibrosis After Myocardial Infarction by Inhibiting CCL5 Expression and the NF-κB Signaling Pathway

Abstract

Purpose Despite significant advances in interventional treatment, myocardial infarction (MI) and subsequent cardiac fibrosis remain major causes of high mortality worldwide. Liquiritin (LQ) is a flavonoid extract from licorice that possesses a variety of pharmacological properties. However, to our knowledge, the effects of LQ on myocardial fibrosis after MI have not been reported in detail. The aim of our research was to explore the potential role and mechanism of LQ in MI-induced myocardial damage. Methods The MI models were established by ligating the left anterior descending branch of the coronary artery. Next, rats were orally administered LQ once a day for 14 days. Biochemical assays, histopathological observations, ELISA, and Western blotting analyses were then conducted. Results LQ improved the heart appearance and ECG, decreased cardiac weight index and reduced levels of cardiac-specific markers such as CK, CK-MB, LDH, cTnI and BNP. Meanwhile, LQ reduced myocardial infarct size and improved hemodynamic parameters such as LVEDP, LVSP and ±dp/dt max . Moreover, H&E staining showed that LQ attenuated the pathological damage caused by MI. Masson staining showed that LQ alleviated myocardial cell disorder and fibrosis while reducing collagen deposition. LQ also decreased the levels of oxidative stress and inflammation. Western blotting demonstrated that LQ significantly down-regulated the expressions of Collagen I, Collagen III, TGF-β1, MMP-9, α-SMA, CCL5, and p-NF-κB. Conclusion LQ protected against myocardial fibrosis following MI by improving cardiac function, and attenuating oxidative damage and inflammatory response, which may be associated with inhibition of CCL5 expression and the NF-κB pathway.

Glycyrrhetinic acid alleviates atrial fibrillation by inhibiting the expression of PIM1

“…Thus, it can be concluded that the incidence and duration of AF can be effectively reduced via repressing fibrosis (Boyle et al., 2021; Heijman et al., 2014). In our study, GA reduced myocardial fibrosis area in a concentration‐dependent manner, analogous to the previous report demonstrating the effects of licorice‐related bioactive substances and compounds on attenuating myocardial fibrosis (Gao, Kan, et al., 2022; Han et al., 2022). Moreover, GA has been documented to exert its anti‐inflammatory effects on AF and to effectively inhibit the expressions of inflammatory factors (IL‐4, IL‐6, IL‐13, and IL‐17).…”

Liquiritin targeting Th17 cells differentiation and abnormal proliferation of keratinocytes alleviates psoriasis via NF‐κB and AP‐1 pathway

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Bioinformatics strategies to identify differences in molecular biomarkers for ischemic stroke and myocardial infarction

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