Key result
Rosmarinic acid-primed exosomes mitigate cardiac fibrosis and improve function in an isoproterenol-induced injury model.
Why the study?
Cardiac fibrosis impairs myocardial function after myocardial infarction, and rosmarinic acid exhibits cardioprotective and antifibrotic properties that may enhance stem cell-derived exosomes.
Do rosmarinic acid-primed exosomes alleviate cardiac fibrosis and improve cardiac function in an isoproterenol-induced myocardial injury model?
Do rosmarinic acid-primed exosomes alleviate cardiac fibrosis and improve cardiac function in an isoproterenol-induced myocardial injury model?
Rosmarinic acid-primed exosomes offer a promising therapeutic strategy for managing myocardial injury and its fibrotic complications by modulating TGF-β1/Smad3 signaling.
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Hypothesis-generating for primed-exosome antifibrotic therapy; leaves open translation to human myocardial injury.
Cardiac fibrosis (CF) is a major complication of myocardial infarction (MI), impairing myocardial function and leading to heart failure. Rosmarinic acid (RA) exhibits cardioprotective and antifibrotic properties, representing a promising therapeutic strategy for CF. This study evaluated the efficacy of exosomes derived from RA‐primed adipose‐derived stem cells (ADSCs), focusing on how RA‐priming enhances their antioxidant and antifibrotic capacity against CF. An Isoproterenol (ISO)‐induced myocardial injury model was established in vitro and in vivo. In vitro, H9C2 cardiomyoblasts were first injured with ISO and then treated with either exosomes (Exo) or RA‐primed exosomes (RA‐MSC‐Exo) to assess cell viability and apoptosis. In vivo, 48 Wistar rats were divided into six groups: Control, Exo, RA‐MSC‐Exo, ISO, ISO + Exo, and ISO + RA‐MSC‐Exo. We assessed cardiac biomarkers (CK‐MB and troponin I), reactive oxygen species (ROS), and total antioxidant capacity (TAC). We performed echocardiographic, molecular (real‐time PCR and Western blotting), and histological analyses (Masson's trichrome staining) to evaluate cardiac function, fibrosis signaling pathways (NF‐κB, TGF‐β1, SMAD3), and collagen deposition. In vitro, both Exo and RA‐MSC‐Exo treatments significantly restored cell viability and reduced apoptosis in ISO‐injured H9C2 cells. In vivo, both treatments significantly mitigated ISO‐induced cardiac injury by reducing cardiac biomarkers, decreasing ROS production, and enhancing TAC levels. These interventions downregulated the expression of NF‐κB, TGF‐β1, Smad3, and Collagen I, leading to attenuated collagen deposition and improved cardiac function. Our study demonstrates that RA‐primed exosomes effectively mitigate CF and improve cardiac function in an ISO‐induced myocardial ischemia model. This targeted approach offers a promising therapeutic strategy for managing myocardial injury and its fibrotic complications.
Mansouri et al. (2026) studied Cardiac fibrosis (n=48). Rosmarinic acid-primed exosomes (RA-MSC-Exo) vs. Exosomes alone, Isoproterenol alone, and Control was evaluated on Cell viability, apoptosis, cardiac biomarkers, ROS, TAC, cardiac function, and fibrosis signaling. Rosmarinic acid-primed exosomes effectively mitigated cardiac fibrosis and improved cardiac function by downregulating NF-κB, TGF-β1, Smad3, and Collagen I in an isoproterenol-induced injury model.
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