Protection
of cardiomyocytes against oxidative stress is vital
to alleviate myocardial ischemia/reperfusion injury (MI/RI). However,
antioxidative treatment is hampered by the lack of safe and effective
therapeutics. Polydopamine (PDA), as a biodegradable class of nanomaterial
with excellent antioxidant properties, has shown great potential in
treating MI/RI. To achieve site-specific antioxidative efficacy, we
established a PDA-based biomimetic nanoplatform (PDA@M), which consisted
of a polydopamine core and a macrophage membrane shell to form a shell–core
structure. By inheriting the inherent migration capability of macrophages,
PDA@M was able to target the infarcted myocardium and exert an antioxidative
effect to protect the myocardium. The results demonstrated that the
accumulation of the membrane-wrapped nanoparticles (NPs) in the infarcted
myocardium was greatly increased as compared with PDA alone, which
effectively relieved the MI/RI-induced oxidative stress. PDA@M largely
decreased the infarct size and improved the cardiac function post-MI/RI.
Our study revealed that PDA@M could inhibit cell pyroptosis by suppressing
the NLRP3/caspase-1 pathway, which is known to play a significant
role in the antioxidant signaling pathway. In summary, PDA@M can target
the infarcted myocardium and exert antioxidative and antipyroptosis
functions to protect the myocardium against MI/RI-induced oxidative
stress, suggesting that it may prove to be a potential therapeutic
agent for MI/RI.
The involvement of cardiomyopathy during sepsis means higher mortality and prolonged length of hospital stay. Many efforts have been made to alleviate the apoptosis of cardiomyocytes in sepsis. The huge potential of IL-13 in tissue repair has attracted increasing attention. In the present study, we used LPS-treated mice or primary cardiomyocytes as a sepsis model to explore the anti-apoptotic ability of IL-13. It was found that an increased level of exogenous IL-13 was beneficial to the recovery of heart function in sepsis, and this anti-apoptotic effect of IL-13 was probably through enhancing the phosphorylation of STAT3 Ser727. In addition, we identified that the heart protective effect of IL-13 was associated with type 2 innate lymphocytes (ILC2). All these findings may provide a potential promising treatment for sepsis-induced cardiomyopathy.
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