What question did this study set out to answer?

This research aims to understand how Ginsenoside Rb1 affects myocardial fibrosis and inflammation through exosomal mechanisms.

March 28, 2026Open Access

Ginsenoside Rb1 Mitigates Myocardial Fibrosis Through Inhibiting Exosomal‐Derived miRNA‐21–Associated Inflammation and Cardiac Signaling

Key Result

Ginsenoside Rb1 attenuates myocardial fibrosis and suppresses inflammatory responses in mice by downregulating exosomal miRNA-21 and reducing the expression of cardiac fibrosis markers.

Key Points

This research aims to understand how Ginsenoside Rb1 affects myocardial fibrosis and inflammation through exosomal mechanisms.
Isolated primary mouse cardiac fibroblasts from neonatal C57BL/6J mice for in vitro assays.
Evaluated Rb1's effects on exosome-derived inflammatory pathways in adult C57BL/6J mice models.
Analyzed gene expression and protein levels using qPCR, Western blotting, and ELISA.
Characterized exosomes using nanoparticle tracking analysis (NTA).
Ginsenoside Rb1 reduced Ang II-induced cell death in cardiac fibroblasts.
Rb1 decreased the expression of fibrosis markers COL1a1, COL3a1, ACTA2, and TGFβ1 in both fibroblasts and mouse models.
Exosomes from fibroblasts had a size range of 80-250 nm, peaking at 149 nm.
Rb1 also inhibited the inflammatory response in the mouse model, as shown by ELISA results.

Structured PICO

Does Ginsenoside Rb1 mitigate myocardial fibrosis and inflammation in Ang II-induced mouse models?

Population

Adult C57BL/6J mice and primary mouse cardiac fibroblasts (pMCFs) isolated from neonatal C57BL/6J mice exposed to Ang II

Intervention

Ginsenoside Rb1

Comparator

Ang II exposure without Ginsenoside Rb1

Outcome

Myocardial fibrosis markers (COL1a1, COL3a1, ACTA2, TGFβ1), inflammatory responses, and exosomal miRNA-21 expressionsurrogate

Ginsenoside Rb1 mitigates Ang II-induced myocardial fibrosis and inflammation by downregulating exosomal miRNA-21 expression in preclinical models.

Main Result

Absolute Event Rate: 0% vs 0%

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.