脓毒性心肌病是脓毒性休克发生的主要原因之一，但其分子机制尚不明确。Siglec-E多表达于单核巨噬细胞表面，我们前期研究显示，脓毒症小鼠巨噬细胞表面Siglec-E升高，且体内干扰Siglec-E后，脓毒症小鼠死亡率明显升高。我们推测Siglec-E参与了脓毒性心肌病的发病过程。课题采用Siglec-E基因敲除小鼠，以盲肠结扎穿孔术制备脓毒症模型，并结合骨髓基质细胞过继性植入，通过超声心动、心肌组织炎症浸润以及心肌细胞凋亡等方面证实Siglec-E对脓毒性心肌病的发病影响；进一步采用NF-κB特异性抑制剂来证实Siglec-E发挥作用受到NF-κB通路的调控。本课题旨在证实Siglec-E通过NF-κB通路调节脓毒性心肌病的发生发展，也证实NF-κB是Siglec-E发挥免疫调节的重要分子通路，为脓毒症治疗提供新方向。

Sepsis induced cardiomyopathy (SIC), as a major participant of septic shock in sepsis, has an ambiguous pathogenesis until now. Siglec-E is a molecular mostly expressed on the surface of macrophage, and our previous study showed that Siglec-E on macrophages in sepsis was up-regulated, and the survival of septic mice decreased when the expression of Siglec-E was inhibited. From those phenomena, we suppose that Siglec-E is involved in the pathogenesis of SIC. Siglec-E knock out mice was employed, and the models of sepsis was prepared by cecal ligation and puncture (CLP). Bone-Marrow Stromal Cells from WT mice was adoptive transferred to animals in vein. After that, echocardiogram, accumulation of Neutrophils and Macrophages in heart tissue, and the apoptosis of cardiomyocyte were tested to confirm the function of Siglec-E. NF-κB inhibitor were used to verify the involvement of NF-κB signal pathway. The purpose of this project is to elucidate that Siglec-E regulates the pathogenesis of SIC through NF-κB signal pathway, which provides a new direction in the treatment of sepsis.