急性特发性血小板减少性紫癜患儿外周血淋巴细胞PPAR-γ mRNA表达变化及其与血浆IL－13的相关性

Correlation of lymphoblastic PPAR-γ mRNA expression with plasma IL-13 contents in children with acute idiopathic thrombocytopenic purpura

目的PPAR-γ与免疫细胞分化、凋亡、增殖和细胞因子分泌调控均密切相关,该实验旨在研究急性特发性血小板减少性紫癜(ITP)患儿外周血淋巴细胞PPAR-γ mRNA表达变化及其与血浆IL-13的相关性。方法序贯收集2007年9月至2008年7月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。RT-PCR法检测ITP患儿外周血淋巴细胞PPAR-γ mRNA的表达,ELISA法检测血浆中IL-13水平。结果急性ITP患儿外周血淋巴细胞PPAR-γ mRNA表达显著高于正常对照组[(0.78±0.03)vs(0.52±0.05),P<0.05];急性ITP患儿血浆中IL-13的含量显著高于正常对照组[(160.21±34.26)pg/mLvs(121.42±12.69)pg/mL,P<0.05]。急性ITP患儿血浆中的IL-13含量与外周血淋巴细胞PPAR-γ mRNA表达变化呈正相关(r=0.89,P<0.05)。结论急性ITP患儿外周血淋巴细胞PPAR-γ mRNA表达上升,并与IL-13水平呈正相关,PPAR-γ与IL-13可能均参与了急性ITP的发病过程。

Objective PPAR-γ is associated with the differentiation, apoptosis, proliferation and cytokine secretion of immunologic cells. This study investigated peripheral blood lymphoblastic PPAR-γ mRNA expression and its correlation with plasma IL-13 contents in children with acute idiopathic thrombocytopenic purpura （1TP）. Methods Fifty-three children with acute ITP who were in line with the standard test between September 2007 and July 2008 were enrolled. Fifty healthy children during the same period were used as the control group. PPAR-γ mRNA expression in peripheral blood lymphocytes were detected by RT-PCR. Plasma IL-13 contents were detected using ELISA. Results PPAR-γ mRNA expression in peripheral blood lymphocytes from acute ITP children were significantly higher than that in the control group （0.78 ± 0.03 vs 0.52 ± 0.05; P 〈0.05）. Plasma IL-13 contents in children with acute ITP were also significantly higher than those in the control group （ 160.21 ± 34.26 pg / mL vs 121.42 ± 12.69 pg / mL; P 〈 0.05 ）. There was a positive correlation between plasma IL-13 level and lymphoblastic PPAR-γ mRNA expression in children with ITP （r = 0.89, P 〈 0.05 ）. Conclusions PPAR-γ mRNA expression in peripheral blood lymphocytes increased and were positively correlated with plasma IL-13 contents in children with acute ITP, suggesting that PPAR-γ and IL-13 might participate in the pathogenesis of acute ITP.