论文部分内容阅读
目的 :通过研究小檗碱对IL - 1、TNF诱导的多形核白细胞 (PMN)与血管内皮细胞粘附及粘附分子表达的影响 ,探讨小檗碱抗炎作用机制。方法 :以小檗碱加IL - 1、TNF处理人PMN或人脐静脉内皮细胞 (HUVEC)后 ,用蛋白染料染色法研究小檗碱对PMN与HUVEC粘附的作用 ,用细胞ELISA、APAAP法研究小檗碱对细胞表面粘附分子表达的影响。结果 :小檗碱与IL - 1或TNF共同处理HUVEC ,能抑制IL - 1、TNF诱导的PMN与HUVEC间的粘附增强 ,且能下调由IL - 1、TNF诱导的HUVEC表面粘附分子ICAM - 1表达的增高 ;小檗碱与TNF共同处理PMN ,能抑制TNF诱导的PMN与HUVEC的粘附增强 ,亦能降低TNF诱导的PMN表面粘附分子CD18的表达。结论 :通过抑制细胞表面粘附分子的表达而抑制PMN与内皮细胞的粘附 ,可能是小檗碱发挥抗炎作用的机制之一。
Objective : To investigate the effect of berberine on the adhesion and adhesion molecule expression of polymorphonuclear leukocytes (PMN) and vascular endothelial cells induced by IL-1 and TNF, and to explore the anti-inflammatory mechanism of berberine. METHODS: After treatment of human PMN or human umbilical vein endothelial cells (HUVEC) with berberine plus IL-1 or TNF, the effect of berberine on the adhesion of PMN to HUVEC was investigated by protein dye staining, using cell ELISA and APAAP method. The effect of berberine on the expression of cell surface adhesion molecules was studied. RESULTS: Treatment of HUVEC with berberine combined with IL-1 or TNF inhibited the adhesion enhancement between PMN and HUVEC induced by IL-1 and TNF, and could down-regulate the adhesion molecule ICAM induced by IL-1 and TNF on HUVEC surface. - 1 increased expression; berberine and TNF co-treatment of PMN, can inhibit TNF-induced adhesion of PMN and HUVEC increased, but also can reduce the TNF-induced PMN surface adhesion molecule CD18 expression. CONCLUSION : The inhibition of PMN adhesion to endothelial cells by inhibiting the expression of adhesion molecules on the cell surface may be one of the mechanisms of berberine in exerting anti-inflammatory effects.