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朱清, 萨仁高娃, 岳欣, 吴明绘. RAS拮抗剂调节血管平滑肌细胞增殖、凋亡因子表达[J]. 中国公共卫生, 2012, 28(5): 633-636. DOI: 10.11847/zgggws2012-28-05-28
引用本文: 朱清, 萨仁高娃, 岳欣, 吴明绘. RAS拮抗剂调节血管平滑肌细胞增殖、凋亡因子表达[J]. 中国公共卫生, 2012, 28(5): 633-636. DOI: 10.11847/zgggws2012-28-05-28
ZHU Qing, SAREN Gao-wa, YUE Xin, . Regulation effects of RAS antagonists on expression of proliferation and apoptosis factor in vascular smooth muscle cells[J]. Chinese Journal of Public Health, 2012, 28(5): 633-636. DOI: 10.11847/zgggws2012-28-05-28
Citation: ZHU Qing, SAREN Gao-wa, YUE Xin, . Regulation effects of RAS antagonists on expression of proliferation and apoptosis factor in vascular smooth muscle cells[J]. Chinese Journal of Public Health, 2012, 28(5): 633-636. DOI: 10.11847/zgggws2012-28-05-28

RAS拮抗剂调节血管平滑肌细胞增殖、凋亡因子表达

Regulation effects of RAS antagonists on expression of proliferation and apoptosis factor in vascular smooth muscle cells

  • 摘要: 目的 探讨血管紧张素转化酶抑制剂卡托普利及血管紧张素Ⅱ(AngⅡ)受体拮抗剂氯沙坦对AngⅡ诱导的肿瘤坏死因子-α(TNF-α)、转化生长因子- β1(TGF- β1)表达的干预作用.方法 体外原代培养Wistar大鼠主动脉平滑肌细胞,收集不同AngⅡ浓度和作用时间下的细胞和卡托普利组、氯沙坦组和二者联合作用组的细胞,以逆转录(RT)-PCR检测细胞中TNF-α和TGF-β1mRNA的表达.结果 TNF-αmRNA表达量随AngⅡ浓度和作用时间增加而增加,AngⅡ浓度为10-7、10-6、10-5、10-4mol/L时表达量分别为(0.43±0.05)、(0.81±0.13)、(0.97±0.17)、(1.09±0.19),与对照组(0.11±0.03)比较,差异有统计学意义(P<0.05或0.01);一定浓度卡托普利(5×10-6mmol/L)、氯沙坦(5×10-6mmol/L)可明显抑制AngⅡ这一作用;TGF- β1mRNA表达量随AngⅡ浓度和作用时间增加而明显增加,具有浓度依赖性;在AngⅡ10-7、10-6、10-5和10-4mol/L时,卡托普利组mRNA表达量分别为(0.19±0.03)、(0.23±0.05)、(0.38±0.14)、(0.34±0.07),较AngⅡ组分别降低了59.57%、73.26%、54.44%和66.67%,差异均有统计学意义(P<0.05或0.01),氯沙坦组分别为(0.17±0.03)、(0.39±0.11)、(0.41±0.12)和(0.39±0.08),较AngⅡ组分别下降了63.82%、54.65%、54.44%和61.76%,差异均有统计学意义(P<0.05).结论 AngⅡ可促进血管平滑肌细胞TNF-α、TGF- β1mRNA表达,且有时间和浓度依赖关系;卡托普利、氯沙坦对AngⅡ诱导的血管平滑肌细胞TNF-α、TGF- β1mRNA表达均有抑制作用,二者联合作用时抑制作用最明显.

     

    Abstract: Objective To investigate the regulation effects of angiotensin converting enzyme inhibitor captopril and AT1 receptor antagonist losartan on expression of tumor necrosis factor-α(TNF-α)and transforming growth factor-β1(TGF-β1)induced by angiotensinⅡ(AngⅡ)in vascular smooth muscle cells.Methods Thoracic aortic vascular smooth muscle cells of male Wistar rats were cultured in vitro.The cultured cells were divided in to control group,AngⅡgroup,captopril group,losartan group,and captopril combined losartan group.Cells in all groups were collected at the culture end point.TNF-αand TGF-β1 mRNA expressions in the collected specimens were detected by reverse transcription-PCR(RTPCR)method,and the effects of AngⅡon TNF-αand TGF-β1 mRNA expression and the regulation of captopril and losartan were observed in different AngⅡconcentrations and different stimulating time in vascular smooth muscle cells.Results TNF-αmRNA expression increased with the increment of AngⅡconcentration and the action time(P<0.05 or P<0.01,except 10-8 mol/L).Captopril(5×10-6 mol/L)and losartan(5×10-6 mol/L)inhibited the action of AngⅡ(P<0.05).The most significant inhibition action occured when capopril combined with losartan(P<0.01).Inhibition effect of losartan on and TNF-αexpression occured later.TNF-αexpression was significantly decreased after 72 hours(P<0.05).TGF-β1 mRNA expression increased with the increment of concentration and the action time of AngⅡ(P<0.01);captopril and losartan decreased the expression of TGF-β1 mRNA(P<0.05 or P<0.01),especially when the two treatments were combined together.Conclusion AngⅡincreases the expressions of TNF-αand TGF-β1 mRNA expression in vascular smooth muscle cells,and the expressions increase with the AngⅡdose and action time.Captopril and losartan inhibit the TNF-α,TGF-β1 mRNA expressions of vascular smooth muscle cells induced by AngⅡ,and the inhibition is the strongest when losartan is combined with captopril.

     

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