NIL10: A New IL10-Receptor Binding Nanoparticle That Induces Cardiac Protection in Mice and Pigs Subjected to Acute Myocardial Infarction through STAT3/NF-kB Activation.
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2022
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Pharmaceutics
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Abstract
Background: Early response after acute myocardial infarction (AMI) prevents extensive
cardiac necrosis, in which inflammation resolution, including expression of anti-inflammatory
interleukin-10 (IL-10), may play a key role. (2) Methods: We synthesized NIL10, a micelle-based
nanoparticle, to target IL-10 receptor in mice and pigs subjected to AMI. (3) Results: Administration
of NIL10 induced cardiac protection of wild-type and IL-10 knockout mice and pigs subjected to AMI.
Cardiac protection was not induced in IL-10-receptor null mice, as shown by a significant recovery of
cardiac function, in which inflammatory foci and fibrosis were strongly reduced, together with the
finding that resolving M2-like macrophage populations were increased after day 3 of reperfusion. In
addition, anti-inflammatory cytokines, including IL-4, IL-7, IL-10, IL-13, IL-16, and IL-27 were also
elevated. Mechanistically, NIL10 induced activation of the IL-10 receptor/STAT-3 signaling pathway,
and STAT3-dependent inhibition of nuclear translocation of pro-inflammatory NF-kB transcription
factor. (4) Conclusions: Taken together, we propose using NIL10 as a novel therapeutic tool against
AMI-induced cardiac damage
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Keywords
Acute myocardial infarction, Interleukin-10, Nanoparticles