Background Patients with unstable angina pectoris and diabetes mellitus are very common. When they receive interventional therapy, contrast agentscan causerenal injuryand platelet activation. Alprostadil has been shown to decrease inflammation and microvascular resistance. There is no any report on the protection effects of alprostadilon renal injuryand the platelet activation during cardiac interventional therapy. Methods A total of 57 patients were divided into two groups, alprostadil group （n=35） and normal group n=22）. BUN （blood urea ni- trogen） and SCr （serum creatine） were measured as the renal function parameters. GFR （glomerular filtration rate） was calculated by the MDRD formula. Platelet parameters： PLT （platelet count, 109）, PDW （platelet distribu- tion width, fL）, MPV （mean platelet volume, fL）, PLCR （large platelet scale ratio, %） were measured as the platelet activationindex. T test and Chi-square test were used as statistical methods, and P〈0.05 was considered statistically significant. Results In the alprostadil group, SCr was 71.1±13.8 μmoFL and 65.9±12.6 ＆tool/L, before and after interventional therapy （P〈0.05）. BUN was 5.68±1.79 mmol/L and 3.86±1.19 mmol/L （P〈0.001）, before and after interventional therapy. I n the platelet tests, MPV was seemed to be the only useful platelet parameter, before and after interventional therapy （11.8±1.8 fL and ll.l±1.2fL, P〈0.05）, while the PLT （109/L）, PDW （fl）, PLCR （%） didn＇ t show any significant difference. In the normal group, all these tests＇ results didn＇ t significantly change after interventional therapy. Conclusions The patients with the unstable angina pectoris and diabetes mellitus have on the risk of renal function damage and platelet activation when undertaking cardiac interventional therapy. Alprostadil protects renal function and alleviates olatelet activation.
目的研究曲格列酮对人单核细胞源性巨噬细胞电压依赖性钾通道Kv1.3、内向整流钾通道Kir2.1表达及膜电位的影响。方法以健康人外周血单核细胞源性巨噬细胞为研究对象,采用Real time RT-PCR及Western blot技术观察曲格列酮对巨噬细胞Kv1.3、Kir2.1表达的调节作用和电压敏感染料膜电位标测技术分析其对巨噬细胞膜电位的影响。结果 50μmol/L曲格列酮显著抑制巨噬细胞Kv1.3的表达,mRNA和蛋白表达下降分别超过82%和60%(P<0.05),而对Kir2.1的表达没有明显影响(P>0.05);同时,巨噬细胞膜电位下降了约23%(P<0.05)。结论曲格列酮分化调节人单核细胞源性巨噬细胞Kv1.3和Kir2.1表达,降低巨噬细胞膜电位。
