抑制继发炎症和减轻二次损伤是脊髓损伤早期的治疗关键之一。脊髓损伤后继发炎症急性期常持续1周，但由于长期静脉使用糖皮质激素会导致多系统并发症，临床上使用糖皮质激素类药物甲基强的松龙常不超过48小时。本项目的前期研究显示，局部释放甲基强的松龙1周可更好得抑制继发炎症，但又对神经系统产生副作用，而局部释放氯化锂可拮抗此副作用。本项目拟利用含有神经细胞粘附分子核心片段（FRM序列）的自组装多肽作为载体，通过特定的化学反应，使之与甲基强的松龙和氯化锂结合。将载药多肽溶液置入大鼠脊髓损伤处，溶液在体内通过自组装形成凝胶,在FRM序列的辅助下贴合在脊髓上，并在局部释放甲基强的松龙和氯化锂1周，以更好得抑制继发炎症和拮抗甲基强的松龙导致的神经系统副作用。本项目为治疗脊髓损伤后继发炎症提供了新思路，具有一定的科学意义和应用前景。

Inhibition of secondary inflammation and subsequent injury is one of the most important strategies for the treatment of early-phase spinal cord injury (SCI). Although secondary inflammation usually lasts more than one week, usage time of methylprednisolone (MP), a synthetic corticosteroid, is limited within 48 hours due to the corticosteroids-induced multiple organ complications and neurotoxicity. Our previous data showed that local controlled-release of MP for 1 week inhibited the secondary inflammation more effectively. However, we also observed MP-induced neurotoxicity, which could be reversed by local delivery of lithium chloride (LiCl). The present study designs and synthesizes a self-assembling peptide containing the neural cell adhesion molecule-derived mimetic peptide FRM. The peptide works as a controlled-releaser of MP and LiCl, after being chemically combined with the two drugs. The soluble drug-containing peptide is then locally delivered onto the lesion site of rats with SCI and releases MP as well as LiCl for 1 week. This may have better effects on inhibition of secondary inflammation and avoid the MP-induced neurotoxicity. The present study may provide a novel approach for inhibition of secondary inflammation after SCI.