An ultrasound activated oxygen generation nanosystem specifically alleviates myocardial hypoxemia and promotes cell survival following acute myocardial infarction.

Hypoxemia after acute myocardial infarction (AMI) causes severe damage to cardiac cells and induces cardiac dysfunction. Protection of cardiac cells and reconstruction of cardiac functions by re-introducing oxygen into the infarcted myocardium represents an efficient approach for the treatment of AMI. However, the established methods for oxygen supplementation mainly focus on systemic oxygen delivery, which always results in inevitable oxidative stress on normal tissues. In this work, an ultrasound (US) activated oxygen generation nanosystem has been developed, which specifically releases oxygen in the infarcted myocardium and alleviates the hypoxemic myocardial microenvironment to protect cardiac cells after AMI. The nanosystem was constructed through the formation of calcium peroxide in the mesopores of biocompatible mesoporous silica nanoplatforms, followed by the assembly of the thermosensitive material heneicosane and polyethyleneglycol. The mild hyperthermia induced by US irradiation triggered the phase change of heneicosane, thus achieving US responsive diffusion of water and release of oxygen. The US-activated oxygen release significantly alleviated the hypoxia and facilitated the mitigation of oxidative stress after AMI. Consequently, the survival of cardiac cells under hypoxic conditions was substantially improved and the damage in the infarcted myocardial tissue was minimized. This US-activated oxygen generation nanosystem may provide an efficient modality for the treatment of AMI.

[The protective effects of curcumin loaded mesoporous silica nanoparticles on rat cardiomyocytes].

Inhibition of apoptosis induced by oxidative stress is an effective way to reduce myocardial injury. In this study, we used H2O2-stimulated rat cardiac myoblast cell line (H9c2) as an oxidative damage model. Curcumin (Cur) was chosen as a model drug and mesoporous silica nanoparticles (MSNs) were chosen as the carrier to construct a Cur-loaded delivery system (Cur@MSNs) and to examine its protective effects against oxidative damage. The MSNs guaranteed efficient loading and controlled release of Cur. Besides, the hydrophilicsilanol groups on the surface of MSNs promoted the Cur solubility in water and increased its cellular uptake amount, which improved the bioavailability of Cur. The results suggest that the Cur@MSNs was pharmacologically active in the reduction of the oxidative damage of H9c2 cells. It was verified that a great decrease of reactive oxygen species was inducted by Cur@MSNs, which led to the protective effects against oxidative damage.