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黄芪甲苷抑制高糖腹透液诱导HMrSV5氧化应激与EMT的实验研究

史俊 俞曼殊 杨劲松 盛梅笑

史俊, 俞曼殊, 杨劲松, 盛梅笑. 黄芪甲苷抑制高糖腹透液诱导HMrSV5氧化应激与EMT的实验研究[J]. 南京中医药大学学报, 2016, 32(4): 337-341.
引用本文: 史俊, 俞曼殊, 杨劲松, 盛梅笑. 黄芪甲苷抑制高糖腹透液诱导HMrSV5氧化应激与EMT的实验研究[J]. 南京中医药大学学报, 2016, 32(4): 337-341.
SHIJun, YUMan-shu, YANGJin-song, SHENGMei-xiao. The Effect of Astragaloside-Ⅳ on Oxygen Stress and EMT of HMrSV5 Induced by High-glucose Peritoneal Dialysate[J]. Journal of Nanjing University of traditional Chinese Medicine, 2016, 32(4): 337-341.
Citation: SHIJun, YUMan-shu, YANGJin-song, SHENGMei-xiao. The Effect of Astragaloside-Ⅳ on Oxygen Stress and EMT of HMrSV5 Induced by High-glucose Peritoneal Dialysate[J]. Journal of Nanjing University of traditional Chinese Medicine, 2016, 32(4): 337-341.

黄芪甲苷抑制高糖腹透液诱导HMrSV5氧化应激与EMT的实验研究

The Effect of Astragaloside-Ⅳ on Oxygen Stress and EMT of HMrSV5 Induced by High-glucose Peritoneal Dialysate

  • 摘要: 目的 观察黄芪甲苷(Astragaloside Ⅳ,AS-Ⅳ)对高糖腹透液诱导人腹膜间皮细胞HMrSV5氧化应激及EMT的影响,探讨ROS在EMT中的作用及AS-Ⅳ干预机制。方法 采用葡萄糖腹透液诱导建立HMrSV5氧化应激模型,相差显微镜观察细胞形态变化,MTT检测AS-Ⅳ及葡萄糖腹透液对细胞活力的影响;予40μg/mL AS-Ⅳ干预HMrSV5氧化应激,DHE荧光探针检测药物作用前后ROS生成水平变化,Western blot检测EMT相关蛋白变化;与ROS清除剂NAC作对照,观察AS-Ⅳ干预HMrSV5氧化应激EMT指标及Smads蛋白的变化。结果 ①40、50μg/mL AS-Ⅳ干预后细胞活力稍有上升(P<0.05);随腹透液作用时间的延长及葡萄糖浓度提高,细胞活力明显抑制,以4.25%高糖腹透液干预48h最明显(P<0.05),细胞拉伸变长;②40μg/mL AS-Ⅳ作用细胞能抑制形态改变,降低模型组ROS的生成(P<0.05),上调E-cadherin、ZO-1表达,下调α-SMA表达,并抑制Smad2/3磷酸化;③5mmol/L NAC产生类似调控作用。结论 高糖腹透液可抑制PMCs细胞活性,增加ROS生成,导致PMCs EMT,其分子机制可能与ROS参与调控的Smads通路激活有关,而AS-Ⅳ可能通过减少ROS生成,抑制Smad2/3磷酸化,阻抑PMCs EMT。

     

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  • 刊出日期:  2016-07-10

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