安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
ACTA UNIVERSITY MEDICINALIS ANHUI
2014年
9期
1253-1257
,共5页
张澄%王峰%冷静%査晚生%张家祥%李树龙%王慧%沈彤%朱启星
張澄%王峰%冷靜%査晚生%張傢祥%李樹龍%王慧%瀋彤%硃啟星
장징%왕봉%랭정%사만생%장가상%리수룡%왕혜%침동%주계성
三氯乙烯%细胞毒性T细胞%BALB/c小鼠
三氯乙烯%細胞毒性T細胞%BALB/c小鼠
삼록을희%세포독성T세포%BALB/c소서
trichloroethylene%cytotoxic T cell%BALB/c mice
目的检测小鼠经三氯乙烯( TCE )致敏后Tc1、Tc2细胞的变化,探讨Tc1/Tc2细胞失衡在三氯乙烯药疹样皮炎( DMLT)中的可能作用。方法 BALB/c雌性小鼠随机分为空白对照、溶剂对照和TCE处理组,在末次激发后24、48、72 h和7d根据皮肤肿胀程度和病理表现分为致敏组和未致敏组。无菌取出脾脏,用流式细胞术检测Tc1、Tc2细胞数量,实时荧光定量PCR检测T-bet、GATA-3 mRNA转录水平。结果与未致敏组相比,致敏组Tc1细胞数量在24、48、72 h和7 d显著上升(P<0.01),72 h水平最高;致敏组Tc2细胞数量在24、48、72 h显著上升(P<0.01),72 h水平达到峰值,7 d较未致敏组差异无统计学意义( P >0.05);致敏组Tc1/ Tc2比例于48、72 h 和7 d 较未致敏组显著上升(P <0.01)。致敏组T-bet、GATA-3 mRNA 转录水平在48、72 h 和7 d 较相应时点未致敏组显著上升(P <0.05,P <0.01),72 h 达到峰值。结论Tc1/ Tc2细胞失衡可能参与了TCE 致敏小鼠的免疫损伤过程并发挥重要的作用。
目的檢測小鼠經三氯乙烯( TCE )緻敏後Tc1、Tc2細胞的變化,探討Tc1/Tc2細胞失衡在三氯乙烯藥疹樣皮炎( DMLT)中的可能作用。方法 BALB/c雌性小鼠隨機分為空白對照、溶劑對照和TCE處理組,在末次激髮後24、48、72 h和7d根據皮膚腫脹程度和病理錶現分為緻敏組和未緻敏組。無菌取齣脾髒,用流式細胞術檢測Tc1、Tc2細胞數量,實時熒光定量PCR檢測T-bet、GATA-3 mRNA轉錄水平。結果與未緻敏組相比,緻敏組Tc1細胞數量在24、48、72 h和7 d顯著上升(P<0.01),72 h水平最高;緻敏組Tc2細胞數量在24、48、72 h顯著上升(P<0.01),72 h水平達到峰值,7 d較未緻敏組差異無統計學意義( P >0.05);緻敏組Tc1/ Tc2比例于48、72 h 和7 d 較未緻敏組顯著上升(P <0.01)。緻敏組T-bet、GATA-3 mRNA 轉錄水平在48、72 h 和7 d 較相應時點未緻敏組顯著上升(P <0.05,P <0.01),72 h 達到峰值。結論Tc1/ Tc2細胞失衡可能參與瞭TCE 緻敏小鼠的免疫損傷過程併髮揮重要的作用。
목적검측소서경삼록을희( TCE )치민후Tc1、Tc2세포적변화,탐토Tc1/Tc2세포실형재삼록을희약진양피염( DMLT)중적가능작용。방법 BALB/c자성소서수궤분위공백대조、용제대조화TCE처리조,재말차격발후24、48、72 h화7d근거피부종창정도화병리표현분위치민조화미치민조。무균취출비장,용류식세포술검측Tc1、Tc2세포수량,실시형광정량PCR검측T-bet、GATA-3 mRNA전록수평。결과여미치민조상비,치민조Tc1세포수량재24、48、72 h화7 d현저상승(P<0.01),72 h수평최고;치민조Tc2세포수량재24、48、72 h현저상승(P<0.01),72 h수평체도봉치,7 d교미치민조차이무통계학의의( P >0.05);치민조Tc1/ Tc2비례우48、72 h 화7 d 교미치민조현저상승(P <0.01)。치민조T-bet、GATA-3 mRNA 전록수평재48、72 h 화7 d 교상응시점미치민조현저상승(P <0.05,P <0.01),72 h 체도봉치。결론Tc1/ Tc2세포실형가능삼여료TCE 치민소서적면역손상과정병발휘중요적작용。
Objective To detect the alterations of Tc1 and Tc2 cells in trichloroethylene ( TCE ) sensitized mice and to shed light on the possible role of Tc1/Tc2 imbalance on occupational medicamentosa-like dermatitis induced by trichloroethylene ( DMLT) . Methods Female BALB/c mice, randomly separated into blank control, solvent control and TCE group, were sacrificed on 24, 48, 72 h and 7 d after last challenge. Sensitized or non-sensitized mice were identified by cutaneous swelling and histological appearance before sacrifice. Spleens were taken to pre-pare splenocyte suspensions quantifying Tc1 and Tc2 by flow cytometry. Tc lineage-specific transcription factors, T-bet and GATA-3, were evaluated by real-time fluorescence quantitative PCR. Results Compared with non-sensi-tized group, the percentages of Tc1 cells in sensitized mice were significantly higher at four consecutive timepoints (P<0.01), which peaked at 72 h. Tc2 cell levels in sensitized mice were markedly elevated at 24 and 48 h with reaching the summit at 72 h ( P<0.01 ) , whereas the level at 7 d showed no significant difference with non-sensi-tized mice ( P>0.05 ) . Tc1/Tc2 ratios in sensitized group were significantly higher at 48 , 72 h and 7 d compared with non-sensitized group. The levels of T-bet and GATA-3 mRNA in sensitized mice were remarkably increased than corresponding non-sensitized mice at 48 , 72 h and 7 d ( P<0.05 , P<0.01 ) . Conclusion The imbalance of Tc1/Tc2 cells may play a key role in the immunological damage in TCE sensitized mice.