羟基磷灰石眶内植入物血管内皮细胞生长因子的表达

目的:探讨血管内皮细胞生长因子(vascular endothelial growth factor,VEGF)与羟基磷灰石(hydroxyapatite,HA)眶内植入物纤维血管化形成的相关性,以及地塞米松抑制羟基磷灰石植入物纤维血管化的机制。方法:家兔20只随机分为实验组与对照组,每组10只;各组均采用HA植入物植入兔眼眶。术后滴妥布霉素滴眼液4次/d,实验组术后48h起隔日球周注射地塞米松0·5mg和实验结束,并观察两组的结膜生长情况;实验组与对照组分别于术后3,7,14,21,28d摘取2只HA植入物行免疫组织化学检测VEGF阳性表达情况。结果:羟基磷灰石植入物纤维血管化与VEGF的表达存在显著的相关性。术后14d,实验组HA炎性细胞浸润明显减少,实验组VEGF表达明显低于对照组。结论:羟基磷灰石植入物纤维血管化与炎症反应密切相关,VEGF可能参与了纤维血管化形成过程,地塞米松可能通过抑制植入物的炎症反应及VEGF的表达。

Expression of vascular endothelial growth factor in hydroxyapatite orbital implants

AIM: To investigate the relevance of formation of fibrovascularization between vascular endothelial growth factor (VEGF) and hydroxyapatite(HA) orbital implants; and the mechanism of dexamethasone suppression on fibrovascularization of HA implants. METHODS: Twenty rabbits were randomly divided into experimental group and control group with 10 in each; each group were used HA implants implanted in rabbit eyes and tobramycine eyedrop was used 4 times per day postoperatively. Peribulbar injection of dexamethasone 0.5mg was applied in the experimental group every other day 48 hours after operation to the end of the experiment, and the growth state of conjunctiva in both groups were observed. 2 HA implants from experimental group and control group respectively were extracted for testing the positive expression of VEGF by immunohistochemistry 3,7,14,21,28 days after operation. RESULTS: There was a significant correlation between HA implants fibrovascularization and the expression of VEGF. Histological examination confirmed that after 14 days, the experimental group HA significantly reduced inflammatory cell infiltration, immunohistochemistry showed that VEGF expression in the experimental group was significantly lower than that in the control group. CONCLUSION: It is closely related between HA implant fibrovascularization and inflammatory reaction; VEGF may be involved in the formation of fibrovascularization, dexamethasone may be through inhibiting the inflamma-tory response and VEGF expression, and thus inhibit implants of fibrovascular growth.