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Updated: Feb 4, 2026
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Live Cell Imaging of the TGF- β/Smad3 Signaling Pathway In Vitro and In Vivo Using an Adenovirus Reporter System
Published on: July 30, 2018
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Rosmarinic Acid-Treated Exosomes Modulate TGF-β1/Smad3 Signaling to Alleviate Cardiac Fibrosis in an In Vitro/In Vivo
Zahra Mansouri1, Mahin Dianat1, Mohammad Badavi1
1Persian Gulf Physiology Research Center, Medical Basic Sciences Research Institute, and Department of Physiology, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Summary
Rosmarinic acid-primed exosomes effectively combat cardiac fibrosis after myocardial injury. This novel therapy improves heart function by reducing oxidative stress and collagen deposition, offering a promising treatment for heart failure.
Area of Science:
- Cardiovascular Biology
- Regenerative Medicine
- Stem Cell Therapy
Background:
- Cardiac fibrosis (CF) is a significant complication of myocardial infarction (MI), leading to impaired heart function and heart failure.
- Rosmarinic acid (RA) demonstrates cardioprotective and antifibrotic effects, making it a potential therapeutic agent for CF.
- Exosomes derived from adipose-derived stem cells (ADSCs) show therapeutic potential, but their efficacy can be enhanced.
Purpose of the Study:
- To evaluate the efficacy of exosomes derived from RA-primed ADSCs (RA-MSC-Exo) in mitigating cardiac fibrosis.
- To investigate how RA-priming enhances the antioxidant and antifibrotic capacity of ADSC-derived exosomes.
- To assess the therapeutic potential of RA-MSC-Exo in an Isoproterenol (ISO)-induced myocardial injury model.
Main Methods:
- Established an in vitro (H9C2 cardiomyoblasts) and in vivo (Wistar rats) ISO-induced myocardial injury model.
- Treated cells and rats with exosomes (Exo) or RA-primed exosomes (RA-MSC-Exo).
- Assessed cell viability, apoptosis, cardiac biomarkers, oxidative stress (ROS, TAC), cardiac function (echocardiography), fibrosis signaling pathways (NF-κB, TGF-β1, Smad3), and collagen deposition (histology).
Main Results:
- Both Exo and RA-MSC-Exo treatments improved cell viability and reduced apoptosis in vitro.
- In vivo, both treatments significantly reduced cardiac biomarkers, decreased ROS, and enhanced TAC levels.
- RA-MSC-Exo and Exo interventions downregulated NF-κB, TGF-β1, Smad3, and Collagen I, attenuated collagen deposition, and improved cardiac function.
Conclusions:
- RA-primed exosomes effectively mitigate cardiac fibrosis and improve cardiac function in a myocardial ischemia model.
- RA-priming enhances the antioxidant and antifibrotic properties of ADSC-derived exosomes.
- This targeted exosome therapy presents a promising strategy for managing myocardial injury and preventing heart failure.
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