临床心血管病杂志
臨床心血管病雜誌
림상심혈관병잡지
JOURNAL OF CLINICAL CARDIOLOGY
2010年
2期
97-100
,共4页
黄斯斯%伍伟锋%林松%黄炎兰
黃斯斯%伍偉鋒%林鬆%黃炎蘭
황사사%오위봉%림송%황염란
心肌病%扩张型%白细胞介素-35%外周血单个核细胞
心肌病%擴張型%白細胞介素-35%外週血單箇覈細胞
심기병%확장형%백세포개소-35%외주혈단개핵세포
cardiomyopathy,dilated%interleukin-35%peripheral blood mononuclear cell
目的:观察白细胞介素-35(IL-35)在扩张型心肌病(DCM)患者外周血单个核细胞(PBMCs)中表达和血浆水平变化,探讨其在DCM发病中的作用.方法:选择对象为30例DCM的患者(DCM组),24例心力衰竭的患者(HF组)及30例健康体检者为正常对照组.用逆转录-聚合酶链反应(RT-PCR)测定PBMCS的IL-35特异性亚基EB病毒诱导基因3(EBI3)mRNA的表达.用酶联免疫吸附法(ELISA)检测血浆中IL-35水平.结果:①DCM组PBMCs表达IL-35的EBI3 mRNA水平(0.15±0.03)明显降低于HF组(0.34±0.08)及正常对照组(0.33±0.07)(均P<0.01),而HF组及正常对照组间差异无统计学意义(P>0.05);②DCM组(24.08±4.40)血浆IL-35的水平明显低于HF组(53.03±5.04)和正常对照组(43.89±8.01)(均P<0.01),而HF组及正常对照组间差异无统计学意义(P>0.05);③DCM组血浆中IL-35含量与射血分数呈正相关(r=0.449,P<0.05),与心功能NYHA分级呈负相关(r=-0.839,P<0.01).结论:DCM患者的IL-35表达下调,提示IL-35可能在DCM的免疫发病机制中起了一定作用.
目的:觀察白細胞介素-35(IL-35)在擴張型心肌病(DCM)患者外週血單箇覈細胞(PBMCs)中錶達和血漿水平變化,探討其在DCM髮病中的作用.方法:選擇對象為30例DCM的患者(DCM組),24例心力衰竭的患者(HF組)及30例健康體檢者為正常對照組.用逆轉錄-聚閤酶鏈反應(RT-PCR)測定PBMCS的IL-35特異性亞基EB病毒誘導基因3(EBI3)mRNA的錶達.用酶聯免疫吸附法(ELISA)檢測血漿中IL-35水平.結果:①DCM組PBMCs錶達IL-35的EBI3 mRNA水平(0.15±0.03)明顯降低于HF組(0.34±0.08)及正常對照組(0.33±0.07)(均P<0.01),而HF組及正常對照組間差異無統計學意義(P>0.05);②DCM組(24.08±4.40)血漿IL-35的水平明顯低于HF組(53.03±5.04)和正常對照組(43.89±8.01)(均P<0.01),而HF組及正常對照組間差異無統計學意義(P>0.05);③DCM組血漿中IL-35含量與射血分數呈正相關(r=0.449,P<0.05),與心功能NYHA分級呈負相關(r=-0.839,P<0.01).結論:DCM患者的IL-35錶達下調,提示IL-35可能在DCM的免疫髮病機製中起瞭一定作用.
목적:관찰백세포개소-35(IL-35)재확장형심기병(DCM)환자외주혈단개핵세포(PBMCs)중표체화혈장수평변화,탐토기재DCM발병중적작용.방법:선택대상위30례DCM적환자(DCM조),24례심력쇠갈적환자(HF조)급30례건강체검자위정상대조조.용역전록-취합매련반응(RT-PCR)측정PBMCS적IL-35특이성아기EB병독유도기인3(EBI3)mRNA적표체.용매련면역흡부법(ELISA)검측혈장중IL-35수평.결과:①DCM조PBMCs표체IL-35적EBI3 mRNA수평(0.15±0.03)명현강저우HF조(0.34±0.08)급정상대조조(0.33±0.07)(균P<0.01),이HF조급정상대조조간차이무통계학의의(P>0.05);②DCM조(24.08±4.40)혈장IL-35적수평명현저우HF조(53.03±5.04)화정상대조조(43.89±8.01)(균P<0.01),이HF조급정상대조조간차이무통계학의의(P>0.05);③DCM조혈장중IL-35함량여사혈분수정정상관(r=0.449,P<0.05),여심공능NYHA분급정부상관(r=-0.839,P<0.01).결론:DCM환자적IL-35표체하조,제시IL-35가능재DCM적면역발병궤제중기료일정작용.
Objective:The aim of this study was to observe the level of interleukin-35(IL-35) in peripheral blood mononuclear cells (PBMCs) with dilated cardiomyopathy (DCM),and explore the role of IL-35 in human DCM. Method:Thirty cases of patients with DCM(DCM group),24 cases of heart failure patients(HF group) and 30 cases of normal adults(NC group) were studied. The subunit EBI3 (Epstein-Barr virus -induced gene 3) of IL-35 mRNA expression in PBMCs were detected by Reverse Transcription-Ploymerase Chain Reaction (RT-PCR). And the level of IL-35 in plasma was measured with Enzyme-linked Immunosorbent Assay (ELISA). Result:①Compared with NC group (0.33±0.07) and HF group (0.34±0.08), the expression of EBI3 mRNA was significantly lower in DCM group (0.15±0.03) in PBMCs (P<0.01).But there was not different between HF group and NC group (P>0.05). ②IL-35 protein level in DCM group (24.08±4.40) was significantly lower compared with NC group (43.89±8.01) and HF group (53.03±5.04). There was a significant difference (P<0.01).But there was not different between HF group and NC group (P>0.05). ③The IL-35 protein level were strongly positively correlated with ejection fraction(r=0.449, P<0.05) of DCM patients, and were negatively correlated with heart function(r=-0.839, P<0.01) of DCM patients.Conclusion:The decrease of IL-35 in DCM, indicated that IL-35 may play an important role in the immune pathogenesis in DCM.
