中文摘要：

目的：观察壳寡糖对脂多糖（LPS）诱导的猪髋动脉内皮细胞（PIECs）炎症损伤的影响以及潜在的分子机制。方法：以脂多糖（1g／mE）＊《激PIECs细胞，建立炎症损伤模型，以RT—PCR和Westernblot的方法观察壳寡糖（COS）预保护PIECs细胞24h，对白介素－8（IL－8）和血管细胞粘附分子．1（VCAM－1）表达水平的影响，以及对JNK信号蛋白磷酸化和c-Fos转录因子表达的影响。结果：壳寡糖可抑制脂多糖刺激的PIECs表达IL－8和VCAM－1，并抑制JNK信号通路的磷酸化和转录因子c-Fos的表达。结论：壳寡糖对脂多糖刺激的PIECs细胞中IL－8和VCAM—1表达的抑制作用是通过抑制上游的JNK信号通路磷酸化和转录因子c-Fos的表达实现的，从而缓解脂多糖对细胞造成的炎症损伤。

英文摘要：

Objective： To investigate the effects of Chitosan oligosaccharides （COS） on lipopolysaccharide （LPS）-induced inflammatory damage in porcine iliac endothelial cells （PIECs） and potential machanisms. Methods： PIECs were pretreated with COS for 24 h followed by LPS （1 g/ml） challenge. Then RT-PCR and Western blot were used to observe the actions of COS on expression ofIL-8 （in- terleukin-8） and Vascular cell adhesion protein 1 （VCAM-1）, phosphorylation ofJNK （Jun N-terminal kinase） signal pathway and activa- tion of nuclear factor c-Fos in LPS-induced PIECs. Results： COS can suppress production of IL-8 and VCAM-1, and can also inhibit phosphorylation of JNK signal pathway and expression of transcription factor c-Fos. Conclusion： COS can exert inhibitory effects on expression of IL-8 and VCAM-1 through blocking phosphorylation of JNK signal protein and production of transcription factor c-Fos upstream in order to inhibit LPS-induced inflammatory injury in PIECs.