水蛭素对血小板源性生长因子及受体的影响

目的 通过观察水蛭素对血小板源性生长因子(PDGF)及受体(PDGF-R)的影响,深入探讨水蛭素防治增生性玻璃体视网膜病变(PVR)形成的机制。方法 利用穿孔性眼外伤的动物模型,分别给予10U/ml和20U/ml的水蛭素于玻璃体腔内,用酶联免疫法(ELISA)测定玻璃体中PDGF的含量,用免疫组织化学法观察玻璃体腔内细胞增殖相关抗原(Ki-67)、白介素1β转换酶(interlukin 1-β converting enzyme,ICE)和PDGFR的表达。结果 造模后3d和28dPDGF的检测结果显示生理盐水对照组(434.88±56,75,457.17±74.39)与剂量Ⅰ组之间(285.95±54.04,322.50±106.93)差异有显著性(P<0.01);PDGF-R的检测结果显示生理盐水对照组(147.82±14.95,141.05±19.03)与剂量Ⅰ组(87.27±20.80,2.57±16.75)和剂量Ⅱ组(97.67±11.37,68.26±5.6)之间差异有显著性(P<0.01);ICE的检测结果显示生理盐水对照组(38.51±3.04,39.74±3.78)与剂量Ⅰ组(57.01±10.02,57.61±9.04)和剂量Ⅱ组(56.22±4.95,57.45±8.25)之间差异有显著性(P<0.01)。Ki-67检测结果显示造模后28d生理盐水对照组(127.83±128.72)与剂量Ⅰ组(51.67±18.61)和剂量Ⅱ组(51.50±31.55)之间差异有显著性(P<0.01和P<0.05)。结论 水蛭素通过抑制PDGF的分泌和PDGF-R的激活而抑制玻璃体腔内细胞的

The effect of Hirudin on platelet-derived growth factor and its receptor

Objective To study the mechanism of Hirudin preventing the formation of PVR by observing the effect of Hirudin on platelet-derived growth factor and its receptor. Methods Rabbit models of penetrating ocular trauma were created by injection of 10 and 20 U/ml of Hiurdin into vitreous cavity respectively, and concentration of platelet-derived growth factor in vitreous cavity were determined by enzyme-linked immunosorbent assay. Expressions of Ki-67, interlukin 1 -3 converting enzyme and platelet-derived growth factor receptor were observed by immunohistochemical staining. Results The levels of platelet-derived growth factor in the 3rd and 28th day was different between control and experimental group I ( P < 0. 01). The level of platelet-derived growth factor receptor showed significant difference between control and experimental group II . The expression of interlukin 1-B converting enzyme was significantly different between control and both experimental groups I and II (P < 0. 01). In the 28th day after the models created, Ki-67 was also found to be significantly different between control group and both experimental group I and II (P <0. 01 ,P <0. 05) . Conclusion By inhibiting the secretion of platelet-derived growth factor and the activation of its receptor,Hirudin prevents the formation of traumatic PVR by suppressing the proliferation of the cell in vitreous cavity,and activating the gene apoptosis.