摘要
目的研究螺旋藻激酶(SPK)对人脐静脉血管内皮细胞通透性及动脉粥样硬化大鼠血清黏附因子的影响。方法体外培养人脐静脉内皮细胞,采用H2O2建立氧化损伤内皮细胞模型。测定单层细胞透过率、细胞外乳酸脱氢酶(LDH)渗出量、细胞分泌的细胞间黏附分子1(ICAM-1)量;采用高脂饲料喂养法建立大鼠动脉粥样硬化(AS)模型,同时给予SPK干预,连续饲养12周。末次给药后取血,分离血清,ELISA法测定细胞间黏附分子1(ICAM-1)、血管细胞黏附分子1(VCAM-1)。结果体外实验:SPK可显著降低氧化损伤造成的单层细胞通透性,减少细胞外溢出的LDH和细胞分泌的ICAM-1(P均<0.05);体内实验:SPK显著降低AS模型大鼠血清ICAM-1、VCAM-1水平(P均<0.05)。结论 SPK可降低血管内皮细胞通透性,减少其释放黏附因子;降低AS大鼠血清黏附因子,预防AS。
Objective To investigate the effects of spirulinakinase（ SPK） on the cell permeability and the adhesion molecules of vascular endothelial cells,and serum adhesion molecules of atherosclerosis（ AS） rats. Methods The human umbilical vein endothelial cells（ HUVECs） were cultured in vitro,and then were induced by hydrogen peroxide（ H2O2） to establish the oxidative damage endothelial cell models. We determined the permeability rate（ T） of monolayer cell and lactate dehydrogenase（ LDH） seepage and intercellular adhesion molecule-1（ ICAM-1）. The rat AS model was established by high-fat diet,and different doses of spirulina kinase（ SPK） were given by gavage. After 12 weeks,rats were killed and the blood serum was collected to measure ICAM-1 and vascular cell adhesion molecule-1（ VCAM-1） by ELISA. Results SPK significantly reduced the oxidative damage-induced permeability of monolayer cell,and the leakage of LDH and the secreted ICAM-1 were decreased in vitro experiment（ all P〈0. 05）; SPK significantly reduced the levels of ICAM-1 and VCAM-1in the serum of AS model rats in vivo experiment（ all P〈0. 05）. Conclusion SPK can decrease the permeability of vascular endothelial cells and reduce the release of adhesion molecules; SPK can decrease the adhesion molecules in serum of AS rats to prevent AS.
出处
《山东医药》
CAS
北大核心
2016年第17期9-12,共4页
Shandong Medical Journal
基金
广西壮族自治区自然科学基金项目(2013GXNSFAA019176)
