Abstract
Background Even though nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling has been associated with the pathogenesis of multiple heart conditions, data on roles of Nrf2 within atrial fibrillation (AF) still remain scant. The present investigation had the aim of analyzing Nrf2-overexpressing role/s upon bone mesenchymal stem cell- (BMSC-) derived exosomes in rats with AF. Methods Exosomes were collected from control or Nrf2 lentivirus-transduced BMSCs and then injected into rats with AF through the tail vein. AF duration was observed using electrocardiography. Immunohistochemical staining was then employed for assessing Nrf2, HO-1, α-SMA, collagen I, or TGF-β1 expression profiles within atrial myocardium tissues. Conversely, Masson staining was utilized to evaluate atrial fibrosis whereas apoptosis within myocardia was evaluated through TUNEL assays. In addition, TNF-α, IL-1β, IL-4, or IL-10 serum expression was assessed through ELISA. Results Results of the current study showed significant downregulation of Nrf2/HO-1 within AF rat myocardia. It was found that injection of the control or Lv-Nrf2 exosomes significantly alleviated and lowered AF timespans together with reducing cardiomyocyte apoptosis. Moreover, injection of Lv-Nrf2 exosomes essentially lowered AF-driven atrial fibrosis and also inhibited inflammatory responses in the rats with AF. Conclusion Delivery of BMSC-derived exosomes using overexpressed Nrf2 inhibited AF-induced arrhythmias, myocardial fibrosis, apoptosis, and inflammation via Nrf2/HO-1 pathway triggering.
Highlights
Atrial fibrillation (AF) is an irregular rhythm of the heart which is mainly characterized by arrhythmia, pulse disorder, palpitation, dizziness, chest discomfort, and shortness of breath [1]
BMSC biomarkers were confirmed through flow cytometry, which was positive for CD29 and CD90 expression but negative for CD45 expression (Figure 1(d))
The current study showed that exosomes from BMSCs protect rats against AF-associated arrhythmias, myocardial fibrosis, apoptosis, and inflammation
Summary
Atrial fibrillation (AF) is an irregular rhythm of the heart which is mainly characterized by arrhythmia, pulse disorder, palpitation, dizziness, chest discomfort, and shortness of breath [1]. The exosomes have multiple pivotal parts within cellular signaling, cell differentiation, immune regulation, metabolic activities, and genomic expression control [7–9]. The present investigation had the aim of analyzing Nrf2-overexpressing role/s upon bone mesenchymal stem cell- (BMSC-) derived exosomes in rats with AF. Exosomes were collected from control or Nrf lentivirus-transduced BMSCs and injected into rats with AF through the tail vein. Masson staining was utilized to evaluate atrial fibrosis whereas apoptosis within myocardia was evaluated through TUNEL assays. Results of the current study showed significant downregulation of Nrf2/HO-1 within AF rat myocardia. Injection of Lv-Nrf exosomes essentially lowered AF-driven atrial fibrosis and inhibited inflammatory responses in the rats with AF. Delivery of BMSC-derived exosomes using overexpressed Nrf inhibited AF-induced arrhythmias, myocardial fibrosis, apoptosis, and inflammation via Nrf2/HO-1 pathway triggering
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
