School of Pharmacy, Hebei University of Chinese Medicine, Shijiazhuang, People's Republic of China.
College of Integrative Medicine, Hebei University of Chinese Medicine, Shijiazhuang, People's Republic of China.
Drug Des Devel Ther. 2022 Dec 2;16:4111-4125. doi: 10.2147/DDDT.S386805. eCollection 2022.
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.
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.
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. 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.
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.
尽管介入治疗取得了重大进展，但心肌梗死（MI）和随后的心脏纤维化仍然是全球高死亡率的主要原因。甘草素（LQ）是从甘草中提取的一种类黄酮，具有多种药理特性。然而，据我们所知，LQ 对 MI 后心肌纤维化的影响尚未详细报道。本研究旨在探讨 LQ 在 MI 引起的心肌损伤中的潜在作用和机制。
通过结扎冠状动脉左前降支建立 MI 模型。然后，大鼠每天口服 LQ 一次，连续 14 天。随后进行生化分析、组织病理学观察、ELISA 和 Western blot 分析。
LQ 改善了心脏外观和心电图，降低了心脏重量指数，降低了心脏特异性标志物如 CK、CK-MB、LDH、cTnI 和 BNP 的水平。同时，LQ 减少了心肌梗死面积，改善了左心室舒张末期压（LVEDP）、左心室收缩压（LVSP）和±dp/dt 等血流动力学参数。此外，H&E 染色显示 LQ 减轻了 MI 引起的病理损伤。Masson 染色显示 LQ 减轻了心肌细胞紊乱和纤维化，同时减少了胶原沉积。LQ 还降低了氧化应激和炎症水平。Western blot 表明，LQ 显著下调了 Collagen I、Collagen III、TGF-β1、MMP-9、α-SMA、CCL5 和 p-NF-κB 的表达。
LQ 通过改善心功能、减轻氧化损伤和炎症反应，对 MI 后心肌纤维化起到保护作用，这可能与抑制 CCL5 表达和 NF-κB 通路有关。
