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.

In in vitro endotoxin tolerant macrophages, the expression of Gfi1 mRNA and protein were up-regulated after high dose LPS stimulation, accompanied with a blunted TNF-alpha and IL-6 secretion. Gfi1 might participate in the mechanism of endotoxin tolerance.

Background Bronchopleural fistula (BPF) is a relatively rare postoperative complication with high mortality. The management is tough and controversial. The aim of this study was to compare the short and long-term outcomes between the conservative and the interventional therapy in postoperative BPF. We also concluded our own strategy and experience of treatment in postoperative BPF. Methods Postoperative BPF patients with malignancies, aged from 18 to 80 years old who had undergone thoracic surgery between June 2011 and June 2020, were included in this study and followed up from 20 months to 10 years. They were retrospectively reviewed and analyzed. Results Ninety-two BPF patients were included in this study, 39 of whom underwent interventional treatment. Significant differences were found in the 28-day and the 90-day survival rates between the conservative and the interventional therapy (P=0.001, 43.40% vs. 76.92%; P=0.006, 35.85% vs. 66.67%). Simple conservative therapy was independently associated with 90-day mortality between the groups in postoperative BPF [P=0.002, hazards ratio (HR) =2.913, 95% confidence interval (CI): 1.480–5.731]. Conclusions Postoperative BPF is notorious for its high mortality. Surgical and bronchoscopic interventions are recommendable in postoperative BPF as they guarantee better short and long-term outcomes compared with the conservative therapy.

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.