机构地区:[1]蚌埠医学院第一附属医院血管外科,安徽蚌埠233004
出 处:《中国临床药理学杂志》2023年第5期639-643,共5页The Chinese Journal of Clinical Pharmacology
摘 要:目的研究七叶皂苷钠(SA)对氧化型低密度脂蛋白(ox-LDL)诱导的血管平滑肌细胞增殖和迁移的影响及其机制。方法将体外培养的人主动脉血管平滑肌细胞(HA-VSMC)随机分为对照组(正常培养不做处理)、模型组(以100μg·mL^(-1)ox-LDL处理24 h)和低、中、高剂量实验组(在ox-LDL处理的基础上分别以0.4,1.6和6.4μg·mL^(-1)的SA处理24 h)。用噻唑蓝(MTT)实验检测细胞增殖,以划痕愈合实验检测细胞迁移,以酶联免疫吸附(ELISA)法检测肿瘤坏死因子α(TNF-α)和超氧化物歧化酶(SOD)水平,用蛋白质印迹法检测蛋白激酶B(Akt)/核因子-κB(NF-κB)信号通路相关蛋白表达。结果对照组、模型组和低、中、高剂量实验组细胞OD450 nm值分别为0.31±0.03、0.90±0.06、0.76±0.06、0.54±0.04、0.36±0.02,迁移率分别为(56.36±3.38)%、(87.02±6.58)%、(78.74±4.55)%、(69.98±3.48)%、(62.68±4.02)%,TNF-α水平分别为(34.59±3.14)、(85.13±5.13)、(74.03±5.47)、(59.40±4.41)、(48.98±3.02)ng·L^(-1),SOD水平分别为(46.52±3.07)、(19.98±1.02)、(26.33±2.19)、(32.30±2.96)、(42.78±3.37)ng·L^(-1),p-Akt/Akt水平分别为0.18±0.02、0.87±0.05、0.73±0.06、0.50±0.04、0.32±0.03,p-p65/p65水平分别为0.12±0.02、0.79±0.05、0.66±0.04、0.45±0.03、0.27±0.03,p-IκBα/IκBα水平分别为0.22±0.03、0.92±0.07、0.80±0.06、0.68±0.03、0.41±0.03;模型组与对照组比较,低、中、高剂量实验组与模型组比较,差异均有统计学意义(均P<0.05)。结论SA可抑制ox-LDL诱导的血管平滑肌细胞增殖和迁移,其作用机制可能与抑制Akt/NF-κB信号通路介导的炎症和氧化应激有关。Objective To investigate the effects of sodium aescinate(SA)on the proliferation and migration of vascular smooth muscle cells induced by oxidized low-density lipoprotein(ox-LDL)and its mechanism.Methods Human aortic vascular smooth muscle cells(HA-VSMC)cultured in vitro were randomly divided into control group(normal culture without treatment),model group(100μg·m L^(-1)oxLDL treatment for 24 h)and low,medium and high dose experimental groupss(treated with 0.4,1.6 and 6.4μg·m L^(-1)SA for 24 h on the basis of ox-LDL treatment).Cell proliferation was detected by thiazolyl blue(MTT)assay and cell migration was detected by wound healing assay.The levels of tumor necrosis factorα(TNF-α)and superoxide dismutase(SOD)were detected by enzymelinked immunosorbent assay(ELISA),and the expression of protein kinase B(Akt)/nuclear factor-κB(NF-κB)signaling pathway related proteins was detected by Western blot.Results The OD450 nmvalues of control group,model group,and low,medium,high dose experimental groups were 0.31±0.03,0.90±0.06,0.76±0.06,0.54±0.04and 0.36±0.02;the migration rates were(56.36±3.38)%,(87.02±6.58)%,(78.74±4.55)%,(69.98±3.48)%,(62.68±4.02)%;TNF-αlevels were(34.59±3.14),(85.13±5.13),(74.03±5.47),(59.40±4.41),(48.98±3.02)ng·L^(-1);SOD levels were(46.52±3.07),(19.98±1.02),(26.33±2.19),(32.30±2.96),(42.78±3.37)ng·L^(-1);p-Akt/Akt levels were 0.18±0.02,0.87±0.05,0.73±0.06,0.50±0.04,0.32±0.03;p-p65/p65 levels were 0.12±0.02,0.79±0.05,0.66±0.04,0.45±0.03,0.27±0.03;p-IκBα/IκBαlevel were 0.22±0.03,0.92±0.07,0.80±0.06,0.68±0.03,0.41±0.03;there were statistically significant differences between model group and control group,between low,medium,high dose experimental groups and model group(all P<0.05).Conclusion SA can inhibit ox-LDL-induced proliferation and migration of vascular smooth muscle cells,which may be related to inhibition of inflammation and oxidative stress mediated by Akt/NF-κB signaling pathway.
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