Myocardial cell mitochondria-targeted mesoporous polydopamine nanoparticles eliminate inflammatory damage in...

Excess reactive oxide species (ROS) is a direct factor in myocardial injury death, thus anti-oxidant therapy is a necessary measure to prevent rapid death of cardiomyocyte cell. Cysteine (Cys) is a potent antioxidant but easily become instability because of the hyperactivity. Therefore, in order to protect the the stability of Cys, we according to the mitochondria are the main sites of ROS production, utilized the loading and ROS scavenging capacity of mesoporous polydopamine (mPDA) constructed a nanosystem targeting mitochondria with effectively ROS elimination capability by loading cysteine (Cys-mPDA@TPP). The mesoporous structure of mPDA effectively inhibited the advance reaction and hyperactivity of Cys, thus effectively improving its stability that reached the double-collaborative treatment excess ROS. In particular, Cys-mPDA@TPP achieved directly reacting with ROS in mitochondria under the targeting of triphenylphosphine (TPP), not only enhancing the elimination efficiency of ROS, but also preventing mitochondrial dysfunction of monocyte-macrophage. Furthermore, with double-collaborative ROS elimination, Cys-mPDA@TPP effectively prevent the damage of cardiomyocyte cell through inhibiting macrophage inflammatory response. Therefore, this study provides a new therapeutic strategy for myocardial inflammatory injury.