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1. 郑州大学第一附属医院肾内科
2. 河南科技大学第一附属医院肾内科
纸质出版日期:2010,
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[1]徐家云,刘章锁,马沙,娄丹,王宜娟,卢丹萍.AngⅡ对大鼠腹膜间皮细胞PAI-1表达的影响及黄芪的干预作用[J].重庆医科大学学报,2010,35(09):1336-1339.
XU Jia-yun, et al. Effects of angiotensin Ⅱ on the expression of rat peritoneum mesothelial cells PAI-1 and and role of astragalus intervention[J]. Journal of Chongqing Medical University, 2010,35(9):1336-1339.
[1]徐家云,刘章锁,马沙,娄丹,王宜娟,卢丹萍.AngⅡ对大鼠腹膜间皮细胞PAI-1表达的影响及黄芪的干预作用[J].重庆医科大学学报,2010,35(09):1336-1339. DOI: 10.13406/j.cnki.cyxb.2010.09.003.
XU Jia-yun, et al. Effects of angiotensin Ⅱ on the expression of rat peritoneum mesothelial cells PAI-1 and and role of astragalus intervention[J]. Journal of Chongqing Medical University, 2010,35(9):1336-1339. DOI: 10.13406/j.cnki.cyxb.2010.09.003.
目的:探讨AngⅡ对腹膜间皮细胞(Peritoneal mesothelial cells
RPMCs)纤溶酶原激活物抑制物(Plasminogen activator inhibitor-1
PAI-1)表达的影响
及二代腹膜间皮细胞经黄芪注射液(Astragelus
AGI)预处理后的干预作用。方法:体外培养SD大鼠原代腹膜间皮细胞至二代
静止24h后
随机分为:正常对照组(A组)
AngⅡ(10-7mol/L)组(B组)
AngⅡ+AG(I2g/ml)组(C组)
AngⅡ+AG(I1g/ml)组(D组)。B组:用AngⅡ(10-7mol/L)体外刺激RPMCs
检测0、2、4、8、12、24h基因水平的变化。C组和D组:分别用AGI(2g/ml)、AGI(1g/ml)预处理后
再行AngⅡ(10-7mol/L)体外刺激RPMCs
基因水平在4h
蛋白水平在24h观察以上各组各指标的变化情况。结果:①AngⅡ以时间依赖方式诱导PAI-1mRNA表达上调
从2h开始
持续至12h
以4h为高峰
为0h的3.51±0.18倍(P<0.05)
AngⅡ可诱导腹膜间皮细胞中PAI-1蛋白表达上调
以24h为高峰
为0h的1.69±0.16倍(P<0.05)。②AGI预处理后可显著阻断这种上调。4h时AGI使PAI-1的mRNA下降了39.43%(C组)
37.28%(D组)
差异具有统计学意义(P<0.05);24h时AGI使PAI-1的蛋白水平下降了29.41%(C组)
24.12%(D组)
差异具有统计学意义(P<0.05)。未观察到AGI对PAI-1的mRNA和蛋白的抑制程度依赖于AGI浓度
即C组与D组比较(P>0.05)。结论:AGI可通过抑制PAI-1的表达
减少腹膜间皮细胞外基质的过度积聚来延缓腹膜纤维化的发生与发展。
Objective:To investigate the role of angiotensin Ⅱ(AngⅡ)and the effects of treatment with astragalus(AGI) on the expression of plasminogen activator inhibitor-1(PAI-1)on rat peritoneal mesothelial cells(RPMCs) Methods:The RPMCs were cultured to the second generation in vitro
and were randomly assigned to the control group(groupA)
the AngⅡ(10-7 mol/L)group(groupB)
the AngⅡ+AGI(2 g/ml) Group(groupC) and the AngⅡ+AGI(1 g/ml) group(groupD).Group B:RPMCs were stimulated with Ang Ⅱ(10-7 mol/L)
RT-PCR was employed to detect the mRNA expression at 0
2
4
8
12
24 h;group C and group D cells were pretreated with AGI 2 g/ml and 1g/ml respectively before adding AngⅡ
and the mRNA expression and protein expression were detected at 4h and 24 h respectively.Results:①AngⅡstimulated PAI-1 mRNA expression in a time-dependent manner from 2 h up to 12 h and peaked at 4h
compared with 0 h group(P< 0.05)
at the same time
PAI-1 protein expression were also upregulated by Ang Ⅱ in RPMCS and peaked at 24 h compared with 0 h(P<0.05).②Treatment with AGI effectively downregulated Ang Ⅱ-induced PAI-1 mRNA and protein overexpression.Ang Ⅱ-induced PAI-1 mRNA overexpression were significantly downregulated by 39.43% and 37.28% with 2 g/ml and 1g/ml AGI treatment respectively after 4 h(P<0.05)
while its protein overexpression were downregulated by 29.41% and 24.12% respectively after 24 h(P<0.05)
and there were no differences of PAI-I expression between the treatment of different AGI concentration(P>0.05).Conclusion:AGI can inhibit the expression of PAI-1
to reduce the accumulation of extracellular matrix in RPMCs and prevent the progression of peritoneal fibrosis.
血管紧张素Ⅱ腹膜间皮细胞纤溶酶原激活物抑制物黄芪
Angiotensin ⅡPerioneal mesothelial cellsPlasninogen activator inhibitor-1Astragalus
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