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作 者:王韶屏[1,2] 游莉[3] 李世英[1,2] 王健[1,2] 杨红[1,2] 程姝娟[1,2]
机构地区:[1]首都医科大学附属北京安贞医院心内科 [2]北京市心肺血管疾病研究所,北京100029 [3]西南大学医院,重庆400715
出 处:《中国药房》2015年第20期2793-2795,共3页China Pharmacy
基 金:国家自然科学基金(青年科学基金)资助项目(No.81000131);北京市自然科学基金资助项目(No.7122058)
摘 要:目的:探讨冠心病患者外周血电压依赖性钾离子通道(KV1.3)和钙离子激活钾通道(KCa3.1)的表达,以及辛伐他汀对其的调控作用。方法:选取冠心病患者20例以及经皮冠脉造影排除冠心病但具有冠心病相关危险因素的对照组患者8例,以实时定量聚合酶链反应(RT-PCR)分别检测两组患者外周血单核细胞KV1.3 m RNA和KCa3.1 m RNA的表达,以及冠心病患者服用辛伐他汀1个月后外周血单核细胞KV1.3 m RNA和KCa3.1 m RNA的表达。结果:与对照组比较,冠心病患者外周血单核细胞KV1.3m RNA的表达水平[(1.54±0.08)vs.(0.77±0.06),P<0.01]和KCa3.1 m RNA的表达水平[(1.32±0.08)vs.(1.06±0.06),P<0.05]均有显著增高。冠心病患者KV1.3 m RNA的表达水平与血浆C反应蛋白(CRP)浓度显著相关(P=0.003),并在患者服用辛伐他汀1个月后表达降低[(1.54±0.08)vs.(1.14±0.05),P<0.01]。而KCa3.1 m RNA的表达水平与血浆CRP浓度不相关,辛伐他汀治疗1个月后其表达也无显著变化。结论:外周血单核细胞KV1.3和KCa3.1可能是冠心病新的标记物,调节外周血单核细胞KV1.3的表达可能是他汀类药物多效性的机制之一。OBJECTIVE: To discuss the expression of voltage-gated potassium channel (KV1.3) and calcium activated potassium channel (KCa3.1) in peripheral monocyte from patients with coronary artery disease (CAD) and the regulatory effect of simvas- tatin. METHODS: 20 patients with CAD and 8 control patients without CAD diagnosed by percutaneous coronary intervention but correlated to risk factor of CAD were enrolled. The expression of KV1.3 mRNA and KCa3.1 mRNA were measured by RT-PCR in 2 groups, and those of CAD group were measured by RT-PCR after 1 month of simvastatin treatment. RESULTS : Compared with control group, mRNA expression of KV1.3 [( 1.54 ± 0.08) vs. (0.77 ± 0.06) ,P〈0.01] and KCa3.1 [( 1.32 ± 0.08) vs. ( 1.06 ± 0.06), P〈0.05] were significantly increased in CAD group, mRNA expression of KV1.3 was significantly correlated to the concentration of C reactive protein (CRP) (P=0.003) and was decreased by simvastatin for one month [(1.54 ± 0.08) vs. (1.14 ± 0.05) ,P〈0.01]. However, mRNA expression of KCa3.1 was not correlated to the concentration of CRP and simvastatin didn' t affect it' s expression. CONCLUSIONS: KV1.3 and KCa3.1 in peripheral monocytes may be two new markers of CAD. Regulating KV1.3 may be one of mechanisms of statin's pleiotrophic effect.
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