Myocardial infarction (MI) is a highly prevalent cardiac emergency, which results in adverse cardiac remodeling and then exacerbates progressive
heart failure. Inflammatory responses in cardiac tissue after MI is necessary for myocardium repair and wound healing. However, the excessive
inflammation is also a key component of subsequent
heart failure pathology. Myoblast
transplantation after MI have been fulfilled attractive effects on cardiac repair, but the complications of
transplantation and the underlying mechanisms have not been fully elucidated. Here, we found that human myoblast
transplantation into minipig myocardium decreased the infiltration of inflammatory cells, the expression levels of many pro-inflammatory genes and the activation of
inflammation-related signal pathways, while upregulated the expression levels of anti-inflammatory genes such as
IL-10 in cardiac tissue of minipig post-MI, which was contributed to the improved cardiac function, the decreased
infarct area and the attenuated myocardial
fibrosis. Moreover, co-culture of human myoblasts inhibited the production of IL-1β and TNF-α as well as activation of MAPK and NF-κB signaling pathway induced by damage-associated molecular patterns such as
HMGB1 and HSP60 in human THP-1 cells, which was partially attributed to the up-regulated production of
IL-10. Collectively, these results indicate that myoblast
transplantation ameliorates
heart injury and improves cardiac function post-MI through inhibiting the inflammatory response, which provides the novel mechanism for myoblast
transplantation therapy of MI.