Engineered Biomimetic Nanoplatform Protects the Myocardium Against Ischemia/Reperfusion Injury by Inhibiting Pyroptosis
| Autor: | Ting Hong, Xumin Hou, Minfang Zhu, Xiaoyu Guo, Yazhong Wei, Yiqiong Liu, Saiqi Li, Bin He, Yongyong Li |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
Male
Cardiac function curve Indoles Materials science Antioxidant Polymers medicine.medical_treatment education Cell Ischemia Myocardial Reperfusion Injury Pharmacology medicine.disease_cause Antioxidants Rats Sprague-Dawley Biomimetic Materials NLR Family Pyrin Domain-Containing 3 Protein Pyroptosis medicine Animals Myocytes Cardiac General Materials Science Macrophages Myocardium Caspase 1 Cell Membrane Heart medicine.disease Oxidative Stress medicine.anatomical_structure cardiovascular system Nanoparticles Signal transduction Reactive Oxygen Species Reperfusion injury Oxidative stress Signal Transduction |
| Zdroj: | ACS Applied Materials & Interfaces. 13:33756-33766 |
| ISSN: | 1944-8252 1944-8244 |
| DOI: | 10.1021/acsami.1c03421 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|