【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(1 g/mL)刺激PIECs细胞,建立炎症损伤模型,以RT-PCR和Western blot的方法观察壳寡糖(COS)预保护PIECs细胞24 h,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。更多还原

【Abstract】 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 of IL-8(interleukin-8) and Vascular cell adhesion protein 1(VCAM-1), phosphorylation of JNK(Jun N-terminal kinase) signal pathway and activation 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.更多还原