当归多糖对氧化型低密度脂蛋白诱导的血管内皮细胞损伤的保护作用研究  

Protective effect of Angelica Sinensis Polysaccharide on oxidized low density lipoprotein induced vascular endothelial cells injury

作　　者：刘琳[1] 柴志勇[1] 刁云辉[1] 李慧[1] 申文宇[1] LIU Lin;CHAI Zhi-yong;DIAO Yun-hui;LI Hui;SHEN Wen-yu(No.1 Cardiovascular Ward,Nanyang Centred Hospital,Nanyang 473000,Henan Province,China)

机构地区：[1]南阳市中心医院心血管内1病区,河南南阳473000

出　　处：《中国临床药理学杂志》2020年第7期818-821,共4页The Chinese Journal of Clinical Pharmacology

摘　　要：目的探讨当归多糖对氧化型低密度脂蛋白(ox-LDL)诱导的血管内皮细胞损伤的保护作用,以及其对血管内皮生长因子(VEGF)-蛋白激酶B(AKT)信号通路的调控机制。方法将人体血管内皮细胞(HUVEC)随机分为空白组,模型组,低、中、高剂量实验组,抑制A、B组。空白组仅给予正常培养;模型组给予200μg·mL-1 ox-LDL处理24 h;低、中、高剂量实验组分别给予10,20,40μmol·L-1当归多糖预处理12 h,然后再给予和模型组相同的处置;抑制A组给予30μmol·L-1 GSK2141795处理30 min,然后给予和中剂量实验组相同的处置;抑制B组给予20μmol·L-1贝伐珠单抗处理30 min,然后给予和中剂量实验组相同的处置。比较7组细胞的乳酸脱氧酶(LDH)的活性、一氧化氮(NO)、细胞凋亡率、VEGF和AKT的表达水平。结果低、中、高剂量实验组和抑制A组、抑制B组、模型组、空白组的LDH分别为(262.56±9.73),(126.20±7.40),(205.74±7.94),(216.99±7.95),(223.78±10.44),(287.06±5.67)和(72.25±1.59)U·L-1,NO分别为(6.30±1.46),(9.21±0.69),(7.21±1.27),(6.92±0.44),(7.42±0.52),(5.92±0.30)和(12.60±0.45)μmol·L-1,细胞凋亡率分别为(18.69±0.52)%,(12.21±1.24)%,(15.79±1.56)%,(16.45±1.34)%,(17.33±1.60)%,(19.47±1.27)%和(4.57±0.46)%,VEGF蛋白表达量分别为(0.51±0.11),(0.67±0.16),(0.58±0.13),(0.12±0.01),(0.61±0.15),(0.32±0.08)和(0.74±0.13),AKT相对表达量分别为(0.73±0.14),(0.92±0.16),(0.77±0.14),(0.12±0.03),(0.07±0.01),(0.51±0.16)和(0.98±0.15),中剂量实验组的上述指标与模型组、抑制A组、抑制B组比较,差异均有统计学意义(均P<0.05)。结论当归多糖对ox-LDL诱导的血管内皮细胞损伤有明显的保护作用,其作用机制与VEGF-AKT信号通路有关。Objective To investigate the protective effect of Angelica Sinensis Polysaccharide on oxidized low-density lipoprotein(ox-LDL)-induced vascular endothelial cell injury and its regulatory mechanism on vascular endothelial growth factor(VEGF)-protein kinase B(AKT) signaling pathway.Methods Human vascular endothelial cells(HUVECs) were divided into blank group, model group, experimental-L,-M and-H groups, inhibitory A and B groups.Blank group was only given normal culture.Model group was treated with 200 μg·mL-1ox-LDL for 24 h.Experimental-L,-M and-H groups were treated with 10,20,and 40 μmol·L-1 Angelica Sinensis Polysaccharide for 12 h,respectively,and then given the same treatment as the model group.Inhibitory A group was treated with 30 μmol·L-1 GSK2141795 for 30 min,and then given the same treatment as the experimental-M group.Inhibitory B group received 20 μmol·L-1 bevacizumab for 30 min,and then given the same treatment as the experimental-M group.The activity of lactate dehydrogenase(LDH),nitric oxide(NO),apoptosis rate and the expression of VEGF and AKT were compared in 7 groups.Results The LDH of blank group,model group,experimental-L,-M and-H groups,inhibitory A and B groups were(262.56±9.73),(126.20±7.40),(205.74±7.94),(216.99±7.95),(223.78±10.44),(287.06±5.67) and(72.25±1.59) U·L-1,NO were(6.30±1.46),(9.21±0.69),(7.21±1.27),(6.92±0.44),(7.42±0.52),(5.92±0.30) and(12.60±0.45) μmol·L-1,apoptosis rates were(18.69±0.52) %,(12.21±1.24) %,(15.79±1.56) %,(16.45±1.34) %,(17.33±1.60) %,(19.47±1.27) % and(4.57±0.46) %,the relative expression of VEGF protein were(0.51±0.11),(0.67±0.16),(0.58±0.13),(0.12±0.01),(0.61±0.15),(0.32±0.08) and(0.74±0.13),the relative expression of AKT protein were(0.73±0.14),(0.92±0.16),(0.77±0.14),(0.12±0.03),(0.07±0.01),(0.51±0.16) and(0.98±0.15),respectively.The above-mentioned indexes in the experimental-M group were significantly different from those in the model group,inhibition A and B groups(all P < 0.05).Conclusion Angelica Sinensis

关 键 词：当归多糖 氧化型低密度脂蛋白 血管内皮生长因子-蛋白激酶B信号通路 血管内皮细胞 

分 类 号：R28[医药卫生—中药学]