中文摘要：

目的：研究阻断ERK途径对地塞米松（DEX）诱导的胸腺细胞凋亡中线粒体膜电势的影响。方法：利用PD098059（PD）阻断小鼠胸腺细胞ERK途径，分别设对照组（control）、单纯PD组（PDonly）、DEX组和PD＋DEX组；在3h、5h和7h时点，利用Annexin V-FITC／PI双染流式细胞术检测细胞凋亡；在3h、7h和11h，利用JC-1染色流式细胞术检测线粒体膜电势（△ψm）变化。结果：在1μmol·L^-1 DEX刺激下，小鼠胸腺细胞在3h、5h和7h凋亡率分别为（19．63±0．35）％、（41．84±1．67）％和（67．00±2．43）％，对照组分别为（4．98±0．39）％、（6．08±0．33）％和（9．31±0．34）％，差异显著（P〈0．01）；相同时点下，PD only组细胞凋亡率分别为（7．95±0．60）％、（10．69±0．48）％和（22．20±1．24）％，显著高于对照组（P〈0．01）；PD＋DEX组在3h和5h时点细胞凋亡率显著高于DEX组（P〈0．01），而在7h时点，两组差异不显著（P〉0．05）。在3h、7h和11h，DEX组△ψm降低的细胞比率分别为（21．23±1．43）％、（55．34±1．78）％和（70．88±2．87）％，对照组分别为（5．25±1．22）％、（8．01±0．97）％和（12．88±1．10）％，差异显著（P〈0．01）；相同时点下，PD only组△ψm降低的细胞比率分别为（11．09±2．00）％、（16．21±2．25）％和（21．15±3．70）％，显著高于对照组（P〈0．01）；PD＋DEX组在3h和5h时点细胞凋亡率显著高于DEX组，分别为（30．55±2．99）％和（65．22±4．32）％（P〈0．01），11h时点两组差异不显著（P〉0．05）。结论：DEX诱导小鼠胸腺细胞凋亡至少部分通过ERK途径，阻断ERK途径在该凋亡过程中具有重要生物学意义。

英文摘要：

AIM： To study the effect of ERK inhibition on the mitochondrial potential change in dexamethasone （DEX） - induced thymocyte apoptosis. METHODS： ERK activity was inhibited by PD098059 （PD）, and 4 experimental groups were set： control, PD only, DEX and PD＋ DEX. Annexin V-FITC/PI double staining flowcytometry was used to detect apoptotic cells at time points of 3 h, 5 h and 7 h. JC - 1 staining flowcytometry was adopted to examine mitochondrial membrane potential （△ψm） at time points of 3 h, 7 h and 11 h. RESULTS： By stimulation with 1μmol/L DEX,,the apoptotic rates of meuse thymocytes at 3 h, 5 h and7 h were （19.63±0.35）%, （41.84±1.67）% and （67.00±2.43）%, respectively, and had significantly difference from control group [ （4.98 ± 0.39 ） %, （ 6.08 ± 0.33 ） % and （ 9.31 ± 0.34） % ] （ P 〈 0.01 ）. At same time points, the rates in PD only group [ （7.95 ± 0.60） %, （ 10.69 ±_ 0.48） % and （22.20 ± 1.24） % ] were higher than that in control group （ P 〈 0.01 ）. Apoptotic.rates in PD ＋ DEX group at 3 h and 11 h were significantly higher than that in DEX group （ P 〈 0.01 ）, and it was of no significance at 7 h （ P 〉 0.05）. At 3 h, 7 h and 11 h, the rates of low △ψm cells were （21.23 ± 1.43）%, （55.34± 1.78）% and （70.88±2.87）%, significantly higher than that in control group （P 〈0.01）. At same time points, the rates in PD group were （ 11.09 ± 2.00） %, （ 16.21 ± 2.25） % and （ 21.15 ± 3.70） %, higher than that in control group （ P 〈 0.01 ）. The rotes in PD ＋ DEX group at 3 h [ （ 30.55 ± 2.99） % ] and 7 h [ （65.22 ± 4.32） % ] were significantly higher than that in DEX group （P〈0.01）, it was of no significance at 11 h （P 〉 0.05）. CONCLUSION： DEX induces mouse thymocyte apoptosis at least partly through ERK pathway, and ERK inhibition has an important biological significance during this process.