凝血酶敏感蛋白2在小鼠角膜碱烧伤后修复过程中的表达

目的观察小鼠角膜碱烧伤后修复过程中凝血酶敏感蛋白2(TSP2)的表达情况。方法制作小鼠角膜碱烧伤模型(实验组,35只)。采用HE染色、免疫组织化学和逆转录聚合酶链反应(RT-PCR)等方法,观察对照组(正常小鼠5只)及实验组小鼠碱烧伤后3、6、12、24、48、96、192h(每时相点5只)角膜组织的形态学改变和TSP2、tsp2的表达情况。结果HE染色显示,实验组小鼠伤后24h起角膜内有明显的血管生成。免疫组织化学和RT-PCR检测结果一致显示,TSP2及tsp2在对照组及实验组小鼠角膜组织中均有表达,多见于上皮层的基底层。与对照组的TSP2表达水平(0.48±0.15)比较,实验组小鼠伤后3h TSP2的表达水平即上升(P<0.05),即6h达第1个峰值1.54±0.45,24h降至低谷0.73±0.19,随后又回升,96h时达第2个峰值1.79±0.63,此后下调,至伤后192h降至对照组水平(P>0.05).tsp2的表达趋势与之相似。结论小鼠角膜碱烧伤后TSP2的表达量随时相点的变化呈波动的趋势,这一变化可能属于应激条件下的代偿性增高。

Expression of thrombospondin 2 during the repair process after alkali burn injury of cornea in mice

OBJECTIVE: To explore the expression of thrombospondin 2 (TSP2) during the repair process after alkali burn injury to cornea in mice. METHODS: Forty mice were employed in the study. The murine corneal alkali burn model was reproduced (n = 35) as experimental group (E), and the mice were randomly divided into control (C, n = 5) and experimental (E, n = 35) groups. The mice in E group were again divided into 7 sub-groups according to different time points 3, 6, 12, 24, 48, 96 and 192 postburn hours (PBHs)] with 5 mice in each sub-group. HE staining, immunocytochemistry (ICC) and RT-PCR were employed to observe the expression of TSP2 in the corneal tissue of mice in both control and all animals in experimental sub-groups at all above mentioned time points (PBHs). RESULTS: TSP2 was expressed in corneal tissue in both C and E groups, especially in the basal layer of epithelial layer, and also a weak expression in substantia propria layer. Compared with that in C group (0.48 +/- 0.15), the expression of TSP2 in E group enhanced at 3 PBH, peaked at 6 PBH, (1.54 +/- 0.45, P < 0.05), dropped to the nadir at 24 PBH (0.73 +/- 0.19), and bounced back afterwards. It peaked again at 96 PBH (1.79 +/- 0.63, P < 0.05), then decreased thereafter, and approached the control level at 192 PBH (P > 0.05). There was remarkable angiogenesis in the cornea at 24 PBH in the mice in E group. CONCLUSION: The expressions of TSP2 exhibits fluctuating changes along with the course of repair. This might be related to the compensatory process under stress condition.