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作 者:王红梅[1,2] 周建明[1,2] 吕耀中[1,2] 周军[1,2] 王振中[1,2] 黄文哲[1,2] 屠鹏飞[3] 萧伟[1,2] WANG Hong-mei1,2, ZHOUJian-ming1,2, LV Yao-zhong1,2 , ZHOU Jun1,2 , WANG Zhen-zhong1,2 , HUANG Wen-zhe1,2, TU Peng-fei3 , XIAO Wei1,2,(1. Jiangsu Kanion Pharmaceutical Co. , Ltd. , Lianyungang 222001, China; 2. State Key Laboratory of New-tech for Chinese Medicine Pharmaceutical Process, Lianyungang 222001, China; 3. School of Pharmacy, Peking University, Beijing 100083, Chin)
机构地区:[1]江苏康缘药业股份有限公司,江苏连云港222001 [2]中药制药过程新技术国家重点实验室,江苏连云港222001 [3]北京大学药学院,北京100083
出 处:《中国中药杂志》2018年第6期1241-1246,共6页China Journal of Chinese Materia Medica
基 金:江苏省“双创计划(双创团队)”项目(苏人才办[2015]26号);江苏省科技成果转化项目(BA2013012)
摘 要:该文为观察龙血通络胶囊对氧化低密度脂蛋白(OX-LDL)致人脐静脉内皮细胞(EAhy.926细胞)损伤的保护作用。采用氧化低密度脂蛋白(100mg·L^-1)损伤建立体外人脐静脉内皮细胞损伤模型方法,MTT法检测龙血通络胶囊对正常细胞生长影响及对损伤细胞的保护作用,酶联免疫吸附法检测龙血通络胶囊对内皮细胞损伤后乳酸脱氢酶(LDH)、一氧化氮(NO)、超氧化物歧化酶(SOD)、丙二醛(MDA)的影响,蛋白质印迹(WB)法检测细胞间黏附分子-1(ICAM-1),血管细胞黏附分子-1(VCAM-1),p65,p-p65,IKB,p-IKB的表达水平。结果显示,与正常对照组比较,OX-LDL损伤后EAhy.926细胞活力显著降低,细胞LDH漏出量增加(P〈0.01),NO含量、SOD活力均显著降低(P〈0.0l,P〈0.05),细胞中MDA含量升高(P〈0.05),ICAM-1,VCAM-1,p-p65/r,65,p-IKB/IKB等蛋白的表达量均显著升高(P〈0.01);与模型对照组比较,龙血通络胶囊(1,2mg·L^-1)对正常细胞生长无显著影响,可促进OX-LDL损伤的血管内皮细胞增殖(P〈0.05,P〈0.01),降低胞内MDA含量、减少细胞LDH释放量(P〈0.05),提高SOD活力及NO含量(P〈0.0l,P〈0.05);可降低ICAM-1,VCAM-1,p-p65/p65,p-IKB/IKB的表达(P〈0.01)。结果提示龙血通络胶囊对OX-LDL所致的人脐静脉内皮细胞损伤具有明显的保护作用,说明龙血通络胶囊对动脉粥样硬化具有一定治疗作用。To observe the protective effect of Longxue Tongluo capsule (LTC) on human umbilical vein endothelial cells (EAhy. 926 cells) injury induced by oxidized low-density lipoprotein ( ox-LDL, 100 mg·L-1 ). The effect of the cell viability of LTCin allevia- ting OX-LDL-induced endothelial cell injury was determined by MrlW and LDH assay. The effect of LTC on lactic dehydrogenase (LDH), nitric oxide (NO), super oxide dlsmutase (SOD) and malondialdehyde (MDA) levels were detected by corresponding assay kits according to manufacturer's instruction. The effect of LTC on the protein expressions of intercellular cell adhesion molecule-t ( ICAM-1 ) , vascular cell adhesion molecule 1 (VCAM-1), p65, p-p65, IKB and p-IKB were detected by Western blot. The results showed that compared with the normal control group, the activity of EAhy. 926 cells was significandy decreased, LDH leakage (P 〈0. 01 ) increased, NO content and SOD activity significantly decreased ( P 〈 0. 01, P 〈 0. 05 ), and the expressions of ICAM-1, VCAM-1, p-p65/p65 and p-IKB ( P 〈 0. 05 ) increased. This study demonstrated that LTC had no significant effect on the growth of nor- mal cells. The treatment with LTC significantly promoted the proliferation of vascular endothelial cells damagedby ox-LDL, decreased MDA content and LDH release, andincreased the activity of SOD and NO content. Meanwhile, ox-LDL significantly increased the ex- pressions of ICAM-1, VCAM-1, p-p65/p65, p-IKB/IKB in Eahy. 926 cells; these effects were suppressed by LTC at 1,2 mg·L-1. In conclusion, LTC has a significant protective effect on human umbilical vein endothelial cells caused by ox-LDL. This study suggested that LTC has a certain therapeutic effect on AS.
关 键 词:龙血通络胶囊 人脐静脉内皮细胞 氧化低密度脂蛋白 MDA SOD LDH NO ICAM-1 VCAM-1 P65 p-p65 IKB p-IKB
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