摘要
目的:观察芍药苷对缺氧损伤的人脐静脉内皮细胞(HUVEC)产生一氧化氮(NO)、内皮型一氧化氮合酶(eNOS)和细胞粘附分子(ICAM-1、VCAM-1)的影响。方法:体外培养HUVEC,传至3代后,以不同浓度的芍药苷分别作用于HUVEC,同时进行缺氧处理。以硝酸还原酶法测定培养液上清中的NO,免疫细胞化学法检测内皮细胞eNOS的表达,细胞ELISA法测定细胞表面ICAM-1和VCAM-1的含量。结果:HUVEC在缺氧48h后产生NO的量显著减少(P<0.001),eNOS表达下调,而ICAM-1、VCAM-1表达上调;芍药苷可以剂量依赖性的增加内皮细胞NO生成量,上调eNOS的表达,下调ICAM-1、VCAM-1表达。结论:芍药苷可能通过增加HUVEC eNOS的表达增加NO的释放、抑制ICAM-1及VCAM-1的表达等途径对内皮细胞起保护作用。
Objective：To investigate the effects of paeoniflorin on the production of nitric oxide （NO）, endothelial nitric oxide synthase （eNOS） and intercellular adhesion molecule - 1 （ ICAM - 1 ）, vasocellular adhesion molecule - 1 （ VCAM - 1 ） in cultured human umbilical vein endothelial ceils （ HUVEC ） under hypoxia. Methods： HUVEC were collected and cultured to the third generation. The hypoxic cell model was established by hypoxia box. The lev- el of NO, eNOS, ICAM - 1 and VCAM - 1 was examined by HNOs reductase method, immunohistochemical method and cell ELISA method, respectively. Results：After HUVEC were cultured under hypoxic condition for 48 h, the production of NO decreased from （85. 263 ±9. 336） μmol · L^-1 to （36. 842 ±6. 316） μmol · L^-1 （P 〈0. 001 ）. Paeoniflorin could enhance the production of NO, increase the expression of eNOS and decrease the expression of ICAM - 1 and VCAM - 1 in HUVEC under hypoxia. Conclusion： Paeoniflorin can protect the function of endothelial cells and enhance the production of NO by activating eNOS as well as decrease the expression of ICAM - 1 and VCAM - 1 in HUVEC under hypoxia.
出处
《药物分析杂志》
CAS
CSCD
北大核心
2007年第4期555-557,共3页
Chinese Journal of Pharmaceutical Analysis
