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Published on: June 3, 2018
Ginsenoside Rb1 Mitigates Myocardial Fibrosis Through Inhibiting Exosomal-Derived miRNA-21-Associated Inflammation
Shihua Wang1, Weifeng Chi1, Yinghong Lu1
1Department of Cardiology, Qingdao Hiser Hospital Affiliated of Qingdao University (Qingdao Traditional Chinese Medicine Hospital), Qingdao, China.
Abstract:
Myocardial fibrosis exemplifies a crucial pathological event in the escalation of heart failure. Natural bioactive agents that can modulate and mitigate myocardial fibrosis hold promising potential as key therapeutic and preventive strategies for managing heart failure. In this study, Ginsenoside Rb1 was found to attenuate myocardial fibrosis and suppress inflammatory responses by downregulating exosomal miRNA-24 expression in the experimental mice models. Primary mouse cardiac fibroblasts (pMCFs) were isolated from neonatal C57BL/6J mice for in vitro assays. For the in vivo investigations, adult C57BL/6J mice were utilized to assess the effects of Rb1 and Ang II on exosome-derived inflammatory pathways. Multiple analytical techniques, including qPCR, Western blotting, nanoparticle tracking analysis (NTA), BrdU staining, and ELISA, were employed to evaluate gene expression, protein levels, exosome characterization, cell proliferation, and cytokine secretion. The obtained results showed that Rb1 prevents Ang II-induced cell death and BrdU-positive cells in the pMCFs. Moreover, we have confirmed that the exosomes derived from pMCF cells have a size range of 80-250 nm, with a peak at 149 nm. RBb-1 prevented the Ang II-exposure-stimulated exosomal mRNA and protein expression of cardiac fibrosis markers (COL1a1, COL3a1, ACTA2, and TGFβ1) in both pMCFs and mice models. Moreover, Rb1 inhibited the inflammatory expression which was confirmed by ELISA. In addition to that, Rb1 impedes the exosomal mRNA expression of miRNA-21 in the mouse model. This study will open up a new insight into the relationship between Rb1 and miRNA-21, which mitigates myocardial fibrosis in the Ang II-induced mouse model.
Insights
Ginsenoside Rb1 mitigates heart failure by reducing myocardial fibrosis and inflammation. It achieves this by downregulating exosomal miRNA-21 expression in mouse models, offering a potential therapeutic strategy.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Pharmacology
Background:
- Myocardial fibrosis is a key factor in heart failure progression.
- Natural compounds offer potential therapeutic avenues for heart failure management.
- Ginsenoside Rb1 is investigated for its cardioprotective effects.
Purpose of the Study:
- To investigate the antifibrotic and anti-inflammatory effects of Ginsenoside Rb1.
- To elucidate the role of exosomal miRNA-21 in Ginsenoside Rb1's mechanism of action.
- To evaluate Ginsenoside Rb1 in an Angiotensin II-induced mouse model of cardiac fibrosis.
Main Methods:
- Primary mouse cardiac fibroblasts (pMCFs) and C57BL/6J mice were used for in vitro and in vivo studies.
- Techniques included qPCR, Western blotting, NTA, BrdU staining, and ELISA.
- Exosome characterization and analysis of fibrosis markers (COL1a1, COL3a1, ACTA2, TGFβ1) and miRNA-21 expression were performed.
Main Results:
- Ginsenoside Rb1 prevented Angiotensin II-induced cell death and proliferation in pMCFs.
- Rb1 inhibited Angiotensin II-induced expression of cardiac fibrosis markers in exosomes from pMCFs and mouse models.
- Rb1 suppressed inflammatory responses and downregulated exosomal miRNA-21 expression in vivo.
Conclusions:
- Ginsenoside Rb1 attenuates myocardial fibrosis and inflammation.
- The mechanism involves the downregulation of exosomal miRNA-21.
- Ginsenoside Rb1 shows promise as a therapeutic agent for heart failure.
