期刊
ACS APPLIED MATERIALS & INTERFACES
卷 13, 期 29, 页码 33756-33766出版社
AMER CHEMICAL SOC
DOI: 10.1021/acsami.1c03421
关键词
myocardial ischemia/reperfusion injury; polydopamine; antioxidative; biomimetic nanoplatform; pyroptosis
资金
- National Natural Science Foundation of China [82072199]
- Clinical Research Plan of SHDC [SHDC2020CR3084B]
- Shanghai Collaborative Innovation Center for Translational Medicine
- Translational Medicine Cross Research Fund of Shanghai Jiaotong University [ZH2018ZDB01, YG2021ZD27, YG2021QN124]
PDA@M, a nanoplatform, can target infarcted myocardium to provide antioxidative and antipyroptosis functions for myocardial protection against MI/RI-induced oxidative stress. The results demonstrate that PDA@M significantly reduces infarct size and improves cardiac function post-MI/RI.
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 nano-particles (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/RIinduced oxidative stress, suggesting that it may prove to be a potential therapeutic agent for MI/RI.
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