强化阿托伐他汀对不稳定型心绞痛患者PCI围术期CD4＋T淋巴细胞SOCS1表达的影响

Effects of aggressive dosing of atorvastatin on the expression of SOCSI in CD4＋ Tlymphocytes from patients with unstable angina pectoris during peri-operative period of PCI

目的探讨强化剂量阿托伐他汀对不稳定心绞痛患者PCI围术期CD4＋T淋巴细胞SOCS1表达的影响。方法人选广西医科大学第一附属医院住院的不稳定型心绞痛患者50例，用随机数字法分为强化他汀组（术前80mg／d，术后40mg／d，n=25）和常规他汀组（术前术后均20mg/d，n=25）。分别于PCI术前、术后18-24h抽取新鲜外周血，免疫磁珠法分选出CD4＋T淋巴细胞，荧光定量PCR检测SOCS1 mRNA表达，蛋白免疫印迹法检测SOCS1蛋白表达，酶联免疫法检测IFN-γ炎症因子的表达。结果①与PCI术前强化组相比，术后强化组SOCSlmRNA、SOCS1蛋白表达明显升高（P〈0．05）。②与PCI术前常规组相比，术后常规组SOCS1 mRNA、SOCSl蛋白表达有升高的趋势，但差异无统计学意义（P〉0．05）③与PCI术前常规组比较，术后常规组血清IFN-γ浓度明显升高（P〈0．05）；与PCI术前强化组比较，术后强化组血清IFN-γ浓度有升高的趋势，但差异无统计学意义（P〉0．05）。结论强化剂量的阿托伐他汀可以通过上调CD4＋T淋巴细胞SOCSl的表达，从而减少PCI术后心肌的炎症反应。

Objective To investigate the effects of aggressive dosing of atorvastatin on the expression of SOCS1 in CD4＋ Tlymphocytes from patients with unstable angina pectoris during peri-operative period of PCI. Methods A cohort of 50 patients with unstable angina pectoris were randomized （ random number） to give pretreatment with either an aggressive dose （80 mg/d, n = 25 ） or a routine dose （ 20 rag/d, n = 25 ） of atorvastatin. Circulating CD4 ＋T cells were subsequently obtained prior to PCI, and also 18 h to 24 hours after PCI, using a magnetic cell sorting system （MACS）. Fluorescence-based quantitative real-time polymerase chain reaction （qRT-PCR） was used to measure expressions of SOCS1 mRNA in the isolated CD4＋ Tlymphocytes, and western blot analysis was used to detect levels of SOCS1 protein. Serum levels of IFN-γ were quantified using enzyme-linked immunosorbent assays （ELISAs）. Results Compared with routine dose group, the expressions of SOCS1 mRNA and protein levels were dramatically increased and those were higher in aggressive dose group following PCI （ P 〈 0. 05 ）. In contrast, serum levels of IFN-γ significantly increased following PCI in both groups, but it was higher in routine dose group than in aggressive dose group （P 〈 0. 05）. Conclusions Treatment with aggressive dosing of atorvastatin reduced the post-PCI myocardial inflammatory response in patients with unstable angina pectoris, possibly modulating by up-regulating SOCS1 expression in CD4＋ Tlymphocytes.