Melatonin Loaded Cardiac Homing Peptide-Functionalized Gold Nanoparticles for the Care of Anti-Cardiac Hypertrophy

Myocardial fibrosis is responsible for the current ineffective treatment of heart hypertrophy. Recent research findings have shown that Melatonin (Mel) reduces heart hypertrophy and fibrosis by promoting sleep and melatonin levels in the body. With the use of poly(lactide) polycarboxy betaine (PLGA-COOH), cardiac homing peptide, and gold nanoparticles (AuNPs), we have developed a unique melatonin delivery and transportation approach via a simple two-step procedure, which we discuss in this study. A mouse model of pressure overdrive cardiac hypertrophy was used to evaluate the effects of nanoparticles (Mel/CHP@AuNPs) on myocardial fibrosis and hypertrophy in the heart. The nanocomposites of Mel/CHP@AuNPs have a diameter of 220.5 ± 4.25 nm and negative zeta potential of 20.18 ± 1.29 mV. An excellent encapsulation capacity for AuNPs (76.12 ± 4.01%) and Melatonin (78.58 ± 5.79%) were found in the Mel/CHP@AuNPs and magnetic characteristics that showed no residual magnetization or coercivity, as demonstrated by the construction of magnetic hysteresis curves. For example, the in vivo echocardiography and real-time polymerase chain reaction (RT-PCR) and histological evaluations demonstrated that Mel/CHP@AuNPs' low dosages improved myocardial hypertrophy and fibrosis. One of the most promising nanoagents for the treatment of cardiac disease is these basic biocompatible, dual-targeting nanoagents.