Effect and Mechanism of Ginsenoside Rg1 Combined with Hirudin in Treating Myocardial Fibrosis in Mice After Acute Myocardial Infarction
10.13422/j.cnki.syfjx.20241208
- VernacularTitle:人参皂苷Rg1联合水蛭素对急性心肌梗死后心肌纤维化小鼠的作用及机制
- Author:
Yi LIU
1
;
Liping CHANG
2
;
Yujie YIN
2
;
Ningxin HAN
1
;
Zhenhua JIA
1
Author Information
1. Graduate School of Hebei Medical University，Shijiazhuang 050017，China
2. National Key Laboratory of Collateral Disease Research and Innovative Traditional Chinese Medicine （TCM），Shijiazhuang 050035，China
- Publication Type:Journal Article
- Keywords:
ginsenoside Rg1;
hirudin;
acute myocardial infarction;
myocardial fibrosis;
endothelial-to-mesenchymal transition
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2024;30(21):86-94
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effect and mechanism of ginsenoside Rg1 （G-Rg1） combined with hirudin in treating myocardial fibrosis in the mouse model of acute myocardial infarction （AMI）. MethodSeventy-five C57BL/6N mice were randomized into sham， model， G-Rg1 （20 mg·kg-1）， hirudin （20 mg·kg-1）， and G-Rg1 （20 mg·kg-1） + hirudin （20 mg·kg-1） groups. The mouse model of AMI was established by ligation of the anterior descending branch of the left coronary artery and continued gavage for 4 weeks. The success of the modeling was judged by ECG changes of mice before and after ligation. The heart weight index， echocardiography， myocardial fibrosis， type Ⅰ collagen α1（COL1A1）， platelet-endothelial cell adhesion molecule-1 （PECAM-1/CD31）， α-smooth muscle actin （α-SMA）， intercellular adhesion molecule-1 （ICAM-1）， and vascular cell adhesion molecule-1 （VCAM-1） were measured before and after treatment. ResultAfter ligation of the anterior descending branch of the left coronary artery， the R wave and T wave merged into a tall tented wave， and the ST segment presented a "damaged" change， indicating that the model was successfully prepared. Compared with the sham group， the model group showed dull and dry hair， slow movement， increased heart weight index （P<0.01）， decreased left ventricular ejection fraction （EF） and left ventricular shortening fraction （FS） （P<0.01）， increased left ventricular end-diastolic diameter （LVEDd） and left ventricular end-systolic diameter （LVESd） （P<0.01）， disarranged myocardial fibers， collagen fiber hyperplasia （P<0.01）， increased expression of COL1A1 （P<0.01）， upregulated protein levels of ICAM-1 and VCAM-1 （P<0.01）， downregulated CD31 expression， and upregulated α-SMA expression （P<0.01）. Compared with the model group， the treatment groups recovered the above indexes in different degrees （P<0.05， P<0.01）， and the combined group had better effect （P<0.05）. ConclusionG-Rg1 combined with hirudin can ameliorate myocardial fibrosis after AMI by inhibiting the expression of adhesion molecular protein in the heart tissue， reducing the adhesion of inflammatory cells， alleviating cardiac inflammation， and inhibiting cardiac endothelial-to-mesenchymal transition.
