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Liquiritin Protects Against Cardiac Fibrosis After Myocardial Infarction by Inhibiting CCL5 Expression and the NF-κB Signaling Pathway.
| Content Provider | Europe PMC |
|---|---|
| Author | Han, Xue Yang, Yakun Zhang, Muqing Li, Li Xue, Yucong Jia, Qingzhong Wang, Xiangting Guan, Shengjiang |
| Copyright Year | 2022 |
| Abstract | PurposeDespite 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.MethodsThe 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.ResultsLQ 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/dtmax. 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.ConclusionLQ 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. |
| Page Count | 15 |
| Volume Number | 16 |
| PubMed Central reference number | PMC9724582 |
| PubMed reference number | 36483459 |
| Journal | Drug Design, Development and Therapy [Drug Des Devel Ther] |
| e-ISSN | 11778881 |
| DOI | 10.2147/DDDT.S386805 |
| Language | English |
| Publisher | Dove |
| Publisher Date | 2022-12-02 |
| Access Restriction | Open |
| Rights License | This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). © 2022 Han et al. |
| Subject Keyword | liquiritin cardiac fibrosis myocardial infarction CCL5 expression NF-κB signaling pathway |
| Content Type | Text |
| Resource Type | Article |
| Subject | Drug Discovery Pharmaceutical Science Pharmacology |
