Cardiotonic Pills® protects from myocardial fibrosis caused by in stent restenosis in miniature pigs

Yan, Lulu; Wei, Xiao‐Hong; Shi, Qiu-Ping; Pan, Chun‐Shui; Li, Kaiyin; Zhang, Bin; Wang, Xingang; Zheng, B.; Wang, Mingxia; Li, Yan; Huang, Ping; Liu, Jian; Fan, Jing‐Yu; Li, Huan; Wang, Chuan-She; Chen, Ming; Han, Jing-Yan

doi:10.1016/j.phymed.2022.154405

Cited by 4 publications

(4 citation statements)

References 24 publications

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Section: Discussionmentioning

confidence: 99%

“…8,56 Yan et al found that MMP-9 expression was increased after MF and was involved in myocardial remodeling after MI. 57 Also, diffuse accumulation of Collagen I and Collagen III in the intercellular matrix causes MF. 58 The results of the Western blotting demonstrated that the expressions of Collagen I and Collagen III were remarkably increased in the MI group rats, accompanied by increased levels of SMA-α, MMP-9 and TGF-β.…”

Section: Discussionmentioning

confidence: 99%

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

Han¹,

Yang²,

Li³

et al. 2022

DDDT

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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.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

Han¹,

Yang²,

Li³

et al. 2022

DDDT

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“…Infarct size was examinate as previously described [ 14 , 15 ]. Briefy, after reperfusion 30 min, pigs were anesthetized, and the hearts were rapidly excised and rinsed with saline, and the ventricular sections were cut into 3–4 mm thick slices evenly parallel to the coronary sulcus.…”

Section: Methodsmentioning

confidence: 99%

Shuangshen Ningxin capsule alleviates myocardial ischemia–reperfusion injury in miniature pigs by modulating mitophagy: network pharmacology and experiments in vivo

Jia,

Chen,

Xin

et al. 2023

Chin Med

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Background Myocardial ischemia/reperfusion injury (MI/RI) is involved in a variety of pathological states for which there is no effective treatment exists. Shuangshen Ningxin (SSNX) capsule which is developed by Xiyuan Hospital, Chinese Academy of Traditional Chinese Medicine has been demonstrated to alleviate MI/RI, but its mechanism remains to be further elucidated. Methods The MI/RI miniature pigs model was constructed to assess the pharmacodynamics of SSNX by blocking the proximal blood flow of the left anterior descending branch of the cardiac coronary artery through an interventional balloon. The principal chemical compounds and potential targets of SSNX were screened by HPLC–MS and SwissTargetPrediction. The targets of MI/RI were identified based on Online Mendelian Inheritance in Man (OMIM) and GeneCards. Cytoscape 3.9.0 was applied to construct a protein–protein interaction (PPI) network, and Gene Ontology (GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were performed using metascape. To further validate the mechanism of SSNX, Molecular docking, Transmission electron microscopy, and Western blot analysis were used to test the effectiveness of targets in related pathways. Results Our results indicated that SSNX significantly improved cardiac function, attenuated myocardial I/R injury. Through network analysis, a total of 15 active components and 201 targets were obtained from SSNX, 75 of which are potential targets for the treatment of MI/RI. KEGG and MCODE analysis showed that SSNX is involved in the mitophagy signaling pathway, and ginsenoside Rg1, ginsenoside Rb1 and ginsenoside Rb2 are key components associated with the mitophagy. Further experimental results proved that SSNX protected mitochondrial structure and function, and significantly reduced the expression of mitophagy-related proteins PTEN-induced putative kinase 1 (PINK1), Parkin, FUN14 domain containing 1 (FUNDC1) and Bcl-2/E1B-19 kDa interacting protein 3 (BNIP3) in MI/RI miniature pigs. Conclusion In our study, the integration of network pharmacology and experiments in vivo demonstrated that SSNX interfered with MI/RI by inhibiting mitophagy.

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“…Calycosin and taohong siwu decoction suppress TGF-β1-induced CFs proliferation and collagen deposition ( Tan et al, 2021 ; Chen et al, 2022a ). Moreover, zerumbone, ganxin V, nutmeg-5, ginsenoside Rg2, jatrorrhizine, cardiotonic pill, and huoxin pill all regulate the TGF-β1/smad pathway to attenuate fibrosis ( Li et al, 2020d ; Wang et al, 2021b ; Yan et al, 2022a ; Yan et al, 2022b ; Li et al, 2022c ; Hao and Jiao, 2022 ; Liang et al, 2022 ). Moreover, citri reticulatae pericarpium also reduces CMs apoptosis, CFs proliferation, and CF-to-MF transformation by upregulating PPAR-γ expression ( Chen et al, 2022c ), while auraptene improves cardiac hypertrophy and dysfunction via activating PPARα ( Sunagawa et al, 2022b ).…”

Section: Interventions For Cardiac Fibrosismentioning

confidence: 99%

Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention

Yin

Pan

et al. 2023

Front. Pharmacol.

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Cardiac fibrosis plays an indispensable role in cardiac tissue homeostasis and repair after myocardial infarction (MI). The cardiac fibroblast-to-myofibroblast differentiation and extracellular matrix collagen deposition are the hallmarks of cardiac fibrosis, which are modulated by multiple signaling pathways and various types of cells in time-dependent manners. Our understanding of the development of cardiac fibrosis after MI has evolved in basic and clinical researches, and the regulation of fibrotic remodeling may facilitate novel diagnostic and therapeutic strategies, and finally improve outcomes. Here, we aim to elaborate pathophysiology, examination and intervention of cardiac fibrosis after MI.

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Cardiotonic Pills® protects from myocardial fibrosis caused by in stent restenosis in miniature pigs

Cited by 4 publications

References 24 publications

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

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

Shuangshen Ningxin capsule alleviates myocardial ischemia–reperfusion injury in miniature pigs by modulating mitophagy: network pharmacology and experiments in vivo

Post-myocardial infarction fibrosis: Pathophysiology, examination, and intervention

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