Ginsenoside Re inhibits myocardial fibrosis by regulating miR-489/myd88/NF-κB pathway
Background: Myocardial fibrosis (MF) is an advanced pathological manifestation of many cardiovascular diseases, which can induce heart failure and malignant arrhythmias. However, the current treatment of MF lacks specific drugs. Ginsenoside Re has anti-MF effect in rat, but its mechanism is still no...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
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Elsevier
2023-03-01
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| Series: | Journal of Ginseng Research |
| Subjects: | |
| Online Access: | http://www.sciencedirect.com/science/article/pii/S1226845321001688 |
| _version_ | 1811162779913027584 |
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| author | Jinghui Sun Ru Wang Tiantian Chao Jun Peng Chenglong Wang Keji Chen |
| author_facet | Jinghui Sun Ru Wang Tiantian Chao Jun Peng Chenglong Wang Keji Chen |
| author_sort | Jinghui Sun |
| collection | DOAJ |
| description | Background: Myocardial fibrosis (MF) is an advanced pathological manifestation of many cardiovascular diseases, which can induce heart failure and malignant arrhythmias. However, the current treatment of MF lacks specific drugs. Ginsenoside Re has anti-MF effect in rat, but its mechanism is still not clear. Therefore, we investigated the anti-MF effect of ginsenoside Re by constructing mouse acute myocardial infarction (AMI) model and AngⅡ induced cardiac fibroblasts (CFs) model. Methods: The anti-MF effect of miR-489 was investigated by transfection of miR-489 mimic and inhibitor in CFs. Effect of ginsenoside Re on MF and its related mechanisms were investigated by ultrasonographic, ELISA, histopathologic staining, transwell test, immunofluorescence, Western blot and qPCR in the mouse model of AMI and the AngⅡ-induced CFs model. Results: MiR-489 decreased the expression of α-SMA, collagenⅠ, collagen Ⅲ and myd88, and inhibited the phosphorylation of NF-κB p65 in normal CFs and CFs treated with AngⅡ. Ginsenoside Re could improve cardiac function, inhibit collagen deposition and CFs migration, promote the transcription of miR-489, and reduce the expression of myd88 and the phosphorylation of NF-κB p65. Conclusion: MiR-489 can effectively inhibit the pathological process of MF, and the mechanism is at least partly related to the regulation of myd88/NF-κB pathway. Ginsenoside Re can ameliorate AMI and AngⅡ induced MF, and the mechanism is at least partially related to the regulation of miR-489/myd88/NF-κB signaling pathway. Therefore, miR-489 may be a potential target of anti-MF and ginsenoside Re may be an effective drug for the treatment of MF. |
| first_indexed | 2024-04-10T06:34:40Z |
| format | Article |
| id | doaj.art-f62170c2598f4dd79a2a4739872f5cd7 |
| institution | Directory Open Access Journal |
| issn | 1226-8453 |
| language | English |
| last_indexed | 2024-04-10T06:34:40Z |
| publishDate | 2023-03-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Journal of Ginseng Research |
| spelling | doaj.art-f62170c2598f4dd79a2a4739872f5cd72023-03-01T04:31:10ZengElsevierJournal of Ginseng Research1226-84532023-03-01472218227Ginsenoside Re inhibits myocardial fibrosis by regulating miR-489/myd88/NF-κB pathwayJinghui Sun0Ru Wang1Tiantian Chao2Jun Peng3Chenglong Wang4Keji Chen5National Clinical Research Center for Chinese Medicine Cardiology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaNational Clinical Research Center for Chinese Medicine Cardiology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaNational Clinical Research Center for Chinese Medicine Cardiology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaInstitute of Integrated Traditional Chinese and Western Medicine, Fujian University of Traditional Chinese Medicine, Fujian, China; Corresponding author. Academy of Integrative Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian, 350122, China.National Clinical Research Center for Chinese Medicine Cardiology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, China; Corresponding author. Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 10091, China.National Clinical Research Center for Chinese Medicine Cardiology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, ChinaBackground: Myocardial fibrosis (MF) is an advanced pathological manifestation of many cardiovascular diseases, which can induce heart failure and malignant arrhythmias. However, the current treatment of MF lacks specific drugs. Ginsenoside Re has anti-MF effect in rat, but its mechanism is still not clear. Therefore, we investigated the anti-MF effect of ginsenoside Re by constructing mouse acute myocardial infarction (AMI) model and AngⅡ induced cardiac fibroblasts (CFs) model. Methods: The anti-MF effect of miR-489 was investigated by transfection of miR-489 mimic and inhibitor in CFs. Effect of ginsenoside Re on MF and its related mechanisms were investigated by ultrasonographic, ELISA, histopathologic staining, transwell test, immunofluorescence, Western blot and qPCR in the mouse model of AMI and the AngⅡ-induced CFs model. Results: MiR-489 decreased the expression of α-SMA, collagenⅠ, collagen Ⅲ and myd88, and inhibited the phosphorylation of NF-κB p65 in normal CFs and CFs treated with AngⅡ. Ginsenoside Re could improve cardiac function, inhibit collagen deposition and CFs migration, promote the transcription of miR-489, and reduce the expression of myd88 and the phosphorylation of NF-κB p65. Conclusion: MiR-489 can effectively inhibit the pathological process of MF, and the mechanism is at least partly related to the regulation of myd88/NF-κB pathway. Ginsenoside Re can ameliorate AMI and AngⅡ induced MF, and the mechanism is at least partially related to the regulation of miR-489/myd88/NF-κB signaling pathway. Therefore, miR-489 may be a potential target of anti-MF and ginsenoside Re may be an effective drug for the treatment of MF.http://www.sciencedirect.com/science/article/pii/S1226845321001688Acute myocardial infarctionAngiotensin ⅡGinsenoside remiR-489Myocardial fibrosis |
| spellingShingle | Jinghui Sun Ru Wang Tiantian Chao Jun Peng Chenglong Wang Keji Chen Ginsenoside Re inhibits myocardial fibrosis by regulating miR-489/myd88/NF-κB pathway Journal of Ginseng Research Acute myocardial infarction Angiotensin Ⅱ Ginsenoside re miR-489 Myocardial fibrosis |
| title | Ginsenoside Re inhibits myocardial fibrosis by regulating miR-489/myd88/NF-κB pathway |
| title_full | Ginsenoside Re inhibits myocardial fibrosis by regulating miR-489/myd88/NF-κB pathway |
| title_fullStr | Ginsenoside Re inhibits myocardial fibrosis by regulating miR-489/myd88/NF-κB pathway |
| title_full_unstemmed | Ginsenoside Re inhibits myocardial fibrosis by regulating miR-489/myd88/NF-κB pathway |
| title_short | Ginsenoside Re inhibits myocardial fibrosis by regulating miR-489/myd88/NF-κB pathway |
| title_sort | ginsenoside re inhibits myocardial fibrosis by regulating mir 489 myd88 nf κb pathway |
| topic | Acute myocardial infarction Angiotensin Ⅱ Ginsenoside re miR-489 Myocardial fibrosis |
| url | http://www.sciencedirect.com/science/article/pii/S1226845321001688 |
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