广东医学
廣東醫學
엄동의학
GUNAGDONG MEDICAL JOURNAL
2009年
12期
1808-1811
,共4页
金呈强%刘仿%张敏%王文涓%宋丽%肖红%郑碧英%陈群%李国明
金呈彊%劉倣%張敏%王文涓%宋麗%肖紅%鄭碧英%陳群%李國明
금정강%류방%장민%왕문연%송려%초홍%정벽영%진군%리국명
急性特发性血小板减少性紫癜%PPAR-γ%IL-18%RT-PCR
急性特髮性血小闆減少性紫癜%PPAR-γ%IL-18%RT-PCR
급성특발성혈소판감소성자전%PPAR-γ%IL-18%RT-PCR
acute idiopathic thrombocytopenic purpura%PPAR-γ%IL-18%RT-PCR
目的 检测急性特发性血小板减少性紫癜(idiopathic thrombocytopenic purpura,ITP)惠儿外周血浆中IL-18对血淋巴细胞PPAR-γ mRNA表达变化影响.方法 序贯收集符合试验入选标准的急性ITP患儿53例,同时收集相匹配的同期体检儿童50例作为对照.将血液标本平均分为5份,在取样1、24、48、72 h后,分别采用RT-PCR法检测ITP患儿外周血淋巴细胞PPAR-γ mRNA的表达,蛋白免疫印迹(western blot)检测PPAR-γ蛋白的含量,ELISA法检测血浆中IL-18水平.结果 急性ITP组白细胞表达PPAR-γ蛋白在1、24、48、72 h与对照组PPAR-γ蛋白分别相比均明显增强,差异有显著性(t_1=7.52,t_(24)=16.38,t_(48)=9.65,t_(72)=12.34,均P<0.05);急性ITP患儿在不同的时间点测定的PPAR-γ mRNA表达水平明显均高于正常对照组(t_1=9.25,t_(24)=14.24,t_(48):8.69,t_(72)=16.14,均P<0.05),同样发现急性ITP患儿血浆IL-18水平均显低于正常对照组(t_1=6.38,t_(24):9.65,t_(48)=8.91,t_(72)=7.19,均P<0.05);血浆IL-18水平与PPAR-γ mRNA表达呈负相关(r=-0.89,P<0.05).结论 血浆中IL-18生成量的减少可能导致了急性ITP患儿外周血淋巴细胞PPAR-γ表达的增加,调控Th1/Th2细胞分化功能出现障碍,使有效的免疫抑制作用降低,导致自身反应性T细胞激活增多、凋亡减少,使得浆细胞产生抗血小板抗体增多,促进了血小板的破坏.
目的 檢測急性特髮性血小闆減少性紫癜(idiopathic thrombocytopenic purpura,ITP)惠兒外週血漿中IL-18對血淋巴細胞PPAR-γ mRNA錶達變化影響.方法 序貫收集符閤試驗入選標準的急性ITP患兒53例,同時收集相匹配的同期體檢兒童50例作為對照.將血液標本平均分為5份,在取樣1、24、48、72 h後,分彆採用RT-PCR法檢測ITP患兒外週血淋巴細胞PPAR-γ mRNA的錶達,蛋白免疫印跡(western blot)檢測PPAR-γ蛋白的含量,ELISA法檢測血漿中IL-18水平.結果 急性ITP組白細胞錶達PPAR-γ蛋白在1、24、48、72 h與對照組PPAR-γ蛋白分彆相比均明顯增彊,差異有顯著性(t_1=7.52,t_(24)=16.38,t_(48)=9.65,t_(72)=12.34,均P<0.05);急性ITP患兒在不同的時間點測定的PPAR-γ mRNA錶達水平明顯均高于正常對照組(t_1=9.25,t_(24)=14.24,t_(48):8.69,t_(72)=16.14,均P<0.05),同樣髮現急性ITP患兒血漿IL-18水平均顯低于正常對照組(t_1=6.38,t_(24):9.65,t_(48)=8.91,t_(72)=7.19,均P<0.05);血漿IL-18水平與PPAR-γ mRNA錶達呈負相關(r=-0.89,P<0.05).結論 血漿中IL-18生成量的減少可能導緻瞭急性ITP患兒外週血淋巴細胞PPAR-γ錶達的增加,調控Th1/Th2細胞分化功能齣現障礙,使有效的免疫抑製作用降低,導緻自身反應性T細胞激活增多、凋亡減少,使得漿細胞產生抗血小闆抗體增多,促進瞭血小闆的破壞.
목적 검측급성특발성혈소판감소성자전(idiopathic thrombocytopenic purpura,ITP)혜인외주혈장중IL-18대혈림파세포PPAR-γ mRNA표체변화영향.방법 서관수집부합시험입선표준적급성ITP환인53례,동시수집상필배적동기체검인동50례작위대조.장혈액표본평균분위5빈,재취양1、24、48、72 h후,분별채용RT-PCR법검측ITP환인외주혈림파세포PPAR-γ mRNA적표체,단백면역인적(western blot)검측PPAR-γ단백적함량,ELISA법검측혈장중IL-18수평.결과 급성ITP조백세포표체PPAR-γ단백재1、24、48、72 h여대조조PPAR-γ단백분별상비균명현증강,차이유현저성(t_1=7.52,t_(24)=16.38,t_(48)=9.65,t_(72)=12.34,균P<0.05);급성ITP환인재불동적시간점측정적PPAR-γ mRNA표체수평명현균고우정상대조조(t_1=9.25,t_(24)=14.24,t_(48):8.69,t_(72)=16.14,균P<0.05),동양발현급성ITP환인혈장IL-18수평균현저우정상대조조(t_1=6.38,t_(24):9.65,t_(48)=8.91,t_(72)=7.19,균P<0.05);혈장IL-18수평여PPAR-γ mRNA표체정부상관(r=-0.89,P<0.05).결론 혈장중IL-18생성량적감소가능도치료급성ITP환인외주혈림파세포PPAR-γ표체적증가,조공Th1/Th2세포분화공능출현장애,사유효적면역억제작용강저,도치자신반응성T세포격활증다、조망감소,사득장세포산생항혈소판항체증다,촉진료혈소판적파배.
Objective To investigate the influence of serum IL-18 on the expression of PPAR-γ mRNA in acute ITP children.Methods Fifty-three acute ITP children who met the cviteria of diagnosis in the hospitals affiliated to Guangdong Medical College from September 2007 to July 2008 were enrolled in the study Fifty healthy children were chosen as controls.Expression of PPAR-γ mRNA on peripheral blood lymphocytes was detected by RT-PCR.Plasma IL-18 was detected by ELISA.Results In acute ITP group,the expression of PPAR-γ protein in leukocyte at 1 h,24h,48 h,72 h were significantly enhanced in comparison with the control group,with significant differences(t_1=7.52,t_(24)=16.38,t_(48)=9.65,t_(72)=12.34,P<0.05);Levels of IL-18 has a negative correlation with the expression of PPAR-γ mRNA(r=-0.89,P<0.05).The expression of PPAR-γ mRNA in acute ITP children were significantly higher than that of the normal control group at different times point(t_1=9.25,t_(24):14.24,t_(48)=8.69,t_(72)=16.14,P<0.05).Plasma IL-18 from children with acute ITP was significantly lower than that of noromal control group(t_1=6.38,t_(24)=9.65,t_(48)=8.91,t_(72)=7.19,P<0.05);Conclusion Reduced plasma IL-18 may lead to increased expression of PPAR-γ on peripheral blood lymphocytes in acute ITP children and impaired Th1/Th2 cell differentiation,which may resuit in self-reactive T cells activation,reduced apoptosis,and increased production of anti-platelet antibodies by plasma cells to promote destruction of platelets.