心肌损伤是脓毒症疾病中最常见的并发症。核因子κB (NF-κB) 的P65亚基在过度炎症反应发生过程中起关键性作用，是治疗心肌损伤的潜在靶点。β1-肾上腺素受体 (β1-AR) 在人体内主要分布在心脏，是纳米粒靶向到心肌细胞的理想靶点。本项目利用RNA干扰技术 (RNAi) 能够沉默特定基因表达的特性以及复合纳米粒材料的靶向性，体外构建β1-AR介导的P65-NF-κB-siRNA心肌细胞靶向纳米粒，并对其表征和性能进行鉴定。 C57BL/6J 小鼠预防性给予P65-NF-κB-siRNA心肌细胞靶向纳米粒，诱导心肌损伤（模型一：腹腔注射脂多糖；模型二：盲肠结扎），观察研究P65-NF-κB-siRNA心肌细胞靶向纳米粒对心肌细胞的保护作用。本研究不仅给基因及药物靶向治疗心肌损伤提供新的途径，也为减少其他脏器损伤的研究和应用提供了新思路。

Myocardial injury is the most commom complication in sepsis. P65 subunit of Nuclear factor kappa B (NF-κB) played a key role in the uncontrolled inflammatory response and was considered as a potential target to protect heart from injury. Beta 1-adrenaline receptors (β1-AR), mainly distributed in the heart in human body, are ideal targets for nanoparticles to target cardiomyocytes. Utilizing the specificity of RNA interference (RNAi) technology to silence specific gene expression and the targeting property of composite nanoparticle materials, β1-AR mediated cardiomyocyte-targetd nanoparticles carried P65-NF-κB-siRNA were constructed in vitro, and their straits and properties were identified. C57BL/6J mice were pretreated with cardiomyocyte-targeted nanoparticles carried P65-NF-κB-siRNA, and then induce myocardial injury (Model 1: injection of LPS intraperitoneally; Model 2: cecum ligation). The protection effect of cardiomyocyte-targeted nanoparticles carried P65-NF-κB-siRNA on myocardial injury was investigated. This study not only provides a new approach to gene and drug targeting therapy for myocardial injury, but also provides a new insight to the research and application of alleviating other organ injuries.