CAJ | 학술논문

目的探讨中国天津地区汉族人群白细胞介素-10(interleukin-10,IL-10)-592C/A基因多态性的功能性以及其对经皮冠状动脉介入治疗(percutaneous coronary intervention,PCI)术后再狭窄的发病,PCI术后血清IL-10水平的影响.方法对437例接受PCI并进行冠状动脉造影随访的患者,按冠状动脉造影结果分为再狭窄组(166例)和非再狭窄组(271例),应用聚合酶链反应-限制性片段长度多态性方法检测IL-10-592位点基因型和等位基因频率的分布;用酶联免疫吸附试验法测定2组PCI术前及PCI术后24 h血清IL-10浓度,并比较两组间和各基因型间IL-10水平.结果 (1)IL-10-592C/A基因型和等位基因频率在再狭窄组和非再狭窄组之间差异无统计学意义(P均＞0.05);(2)PCI术后24 h血清IL-10水平再狭窄组显著低于非再狭窄组[(82.67±35.02)ng/Lvs.(95.08±32.26)ng/L,P＜0.05];(3)IL-10-592位点A等位基因携带者(AA+AC基因型)术后24 h血清IL-10水平明显低于非携带者(CC型)[(86.13±34.77)ng/L vs.(102.50±27.52)ng/L,P＜0.05];(4)再狭窄组A等位基因携带者术后24 h血清IL-10水平明显低于非携带者[(78.51±34.09)ng/L vs.(102.19±33.66)ng/L,P＜0.05];(5)再狭窄危险的多因素Logistie回归分析显示:急性冠状动脉综合征、术前狭窄程度、靶病变长度与冠状动脉内支架再狭窄呈正相关(()R值分别为5.90、1.86、2.83),术后24 h血清IL-10水平、参照血管直径、支架直径与冠状动脉内支架再狭窄呈负相关(OR值分别为0.99、0.70、0.46).结论 (1)IL-10基因-592 C/A多态性与中国天津地区汉族人群再狭窄发病无关;(2)IL-10是PCI术后早期的炎症细胞因子,术后24 h血清IL-10水平为再狭窄的独立预测因素,携带A等位基因的个体可能通过降低其表型血清IL-10水平而增加了冠状动脉内支架术后再狭窄的发病.
목적 탐토중국천진지구한족인군백세포개소-10(interleukin-10,IL-10)-592C/A기인다태성적공능성이급기대경피관상동맥개입치료(percutaneous coronary intervention,PCI)술후재협착적발병,PCI술후혈청IL-10수평적영향.방법 대437례접수PCI병진행관상동맥조영수방적환자,안관상동맥조영결과분위재협착조(166례)화비재협착조(271례),응용취합매련반응-한제성편단장도다태성방법검측IL-10-592위점기인형화등위기인빈솔적분포;용매련면역흡부시험법측정2조PCI술전급PCI술후24 h혈청IL-10농도,병비교량조간화각기인형간IL-10수평.결과 (1)IL-10-592C/A기인형화등위기인빈솔재재협착조화비재협착조지간차이무통계학의의(P균＞0.05);(2)PCI술후24 h혈청IL-10수평재협착조현저저우비재협착조[(82.67±35.02)ng/Lvs.(95.08±32.26)ng/L,P＜0.05];(3)IL-10-592위점A등위기인휴대자(AA+AC기인형)술후24 h혈청IL-10수평명현저우비휴대자(CC형)[(86.13±34.77)ng/L vs.(102.50±27.52)ng/L,P＜0.05];(4)재협착조A등위기인휴대자술후24 h혈청IL-10수평명현저우비휴대자[(78.51±34.09)ng/L vs.(102.19±33.66)ng/L,P＜0.05];(5)재협착위험적다인소Logistie회귀분석현시:급성관상동맥종합정、술전협착정도、파병변장도여관상동맥내지가재협착정정상관(()R치분별위5.90、1.86、2.83),술후24 h혈청IL-10수평、삼조혈관직경、지가직경여관상동맥내지가재협착정부상관(OR치분별위0.99、0.70、0.46).결론 (1)IL-10기인-592 C/A다태성여중국천진지구한족인군재협착발병무관;(2)IL-10시PCI술후조기적염증세포인자,술후24 h혈청IL-10수평위재협착적독립예측인소,휴대A등위기인적개체가능통과강저기표형혈청IL-10수평이증가료관상동맥내지가술후재협착적발병.
Objective To investigate the relationship of interleukin-10 gene (IL-10)polymorphism and the serum IL-10 level with restenosis after percutaneous coronary intervention (PCI) in Tianjin Chinese Han population and study the effect of IL-10 gene polymorphism on serum IL-10 level. Methods Four hundred and thirty-seven patients who successfully underwent PCI with a follow-up angiography were divided into a restenosis group (n= 166) and non-restenosis group (n= 271). The IL-10 gene promoter polymorphism at position -592 was determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Meanwhile their serum IL-10 level before and 24 h after PCI was determined by enzyme-linked immunosorbent assay (ELISA). Results (1) There was no significant difference in frequencies of -592 genotypes and alleles between the two groups (P＞0. 05); (2) The 24 hpost-PCI IL-10 serum level of restenosis group was significantly lower than that of the non-restenosis group [(82. 67±35. 02) ng/L vs. (95.08±32.26) ng/L, P＜0.05]; (3) The serum level of the A allele carriers (AA+AC) was significant lower than that of the CC carriers [(86.13±34.77) ng/L vs. (102. 50±27.52)ng/L,P＜0.05]; (4) In the restenosis group, the 24 h post-PCI serum level of IL-10 in the A allele carriers was also significantly lower than that in those without the A allele [(78.51 ± 34.09) ng/L vs. (102.19 ±33.66) ng/L, P＜ 0. 05]; (5) Logistic regression analysis revealed positive correlations between acute coronary syndrome patients, pre-PCI degree of stenosis, length of target stenosis lesion and restenosis (OR=5.90, 1.86, 2.83 respectively); and there were negative correlations between 24 h post-PCI serum level of IL-10, the stent diameter, the diameter of reference vessel before stent implantation and restenosis (OR=0. 99, 0. 70, 0. 46 respectively). Conclusion (1) TheIL-10 gene -592 C/A polymorphism was not associated with restenosis in the Tianjin Chinese Han population; (2) IL-10 is an early post-PCI inflammatory cytokine, 24 h post-PCI serum IL-10 level was an independent predictive factor for restenosis,the IL-10 A allele carriers may have increased incidence of in-stent restenosis (ISR) by reducing the serum IL-10 levels.