Abstract
Ischemic heart disease is the main cause of death globally. Cardioprotection is the process whereby mechanisms that reduce myocardial damage, and activate protective factors, contribute to the preservation of the heart. Targeting these processes could be a new strategy in the treatment of post-ischemic heart failure (HF). Triiodothyronine (T3) and thyroxine (T4), which have multiple effects on the heart, prevent myocardial damage. This study describes the formulation, and characterization, of chemically modified polymeric nanoparticles incorporating T3, to target the thyroid hormone receptors. Modified T3 was conjugated to polylactide-co-glycolide (PLGA) to facilitate T3 delivery and restrict its nuclear translocation. Modified T3 and PLGA-T3 was characterized with 1H-NMR. The protective role of synthesized phosphocreatine (PCr) encapsulated PLGA-T3 nanoparticles (PLGA-T3/PCr NPs) and PLGA-T3 nanoparticles (PLGA-T3 NPs) in hypoxia-mediated cardiac cell insults was investigated. The results showed that PLGA-T3/PCr NPs represent a potentially new therapeutic agent for the control of tissue damage in cardiac ischemia and resuscitation.
Highlights
Cardioprotection is a wide-ranging term that includes all mechanisms for the protection of the heart, and the multiple factors involved, such as cardiomyocytes, cytokines, cell growth, angiogenesis, and mitochondria
0.001 versus control untreated, with full reversal and improvement versus control under normoxic condi*** p < 0.001 versus control untreated, with full reversal and improvement versus control under normoxic condition.These tion.These results suggest that of PLGA-T3 NPs and PLGA-T3 NPs/PCr inhibit the damaging effect of hypoxia on cardioresults suggest that of PLGA-T3 NPs and PLGA-T3 NPs/PCr inhibit the damaging effect of hypoxia on cardiomyocytes
We aimed to develop T3 conjugated PLGA-T3 NP to of therapeutic agents
Summary
Cardioprotection is a wide-ranging term that includes all mechanisms for the protection of the heart, and the multiple factors involved, such as cardiomyocytes, cytokines, cell growth, angiogenesis, and mitochondria. T3, the most active form of thyroid hormone, is involved in cardiac protection through several mechanisms. Through nongenomic actions it interacts with cytoplasmic and membrane-associated thyroid hormone receptors, namely the integrin, αvβ, and mediates the action of thyroid hormone on the ion channels located in the cardiomyocyte membrane [4,5], to protect cells from ischemic injury [6]. By this action, T3 activates the cell surface receptor integrin αvβ and leads to the formation of new blood vessels (angiogenesis)
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