[关键词]
[摘要]
目的:观察青光眼小梁切除术后晶状体细胞抗氧化酶活性的变化,探讨青光眼术后白内障的发病机制。
方法:新西兰白兔16只32眼,左眼行小梁切除术为治疗组,右眼未手术作为正常对照组。术后定期观察晶状体混浊情况,6mo后取出晶状体行Na+-K+-ATP酶、过氧化氢酶(CAT)、超氧化物歧化酶(SOD)、谷胱甘肽还原酶(GR)、谷胱甘肽过氧化物酶(GSH-Px)的活性以及脂质过氧化反应终产物丙二醛(MDA)的含量检测。
结果:6mo后,治疗组晶状体在透明度和组织形态学上与正常对照组差异无统计学意义(P>0.05),治疗组与正常对照组相比,晶状体Na+-K+-ATP酶、CAT,SOD,GR,GSH-Px活性分别下降了20.97%,16.36%,4.46%,4.85%和10.02%,差异均有统计学意义(P<0.05),与正常对照组相比,治疗组的MDA含量升高了16.31%,差异有统计学意义(P<0.05)。
结论:小梁切除术可使成年兔晶状体发生生物化学改变,对研究青光眼滤过术后白内障的发生发展机制有重要的指导意义。
[Key word]
[Abstract]
AIM: To observe the change of lens antioxidant enzyme activity after glaucoma trabecular resection.
METHODS: Thirty-two eyes of sixteen New-Zealand rabbits(2.2-2.4kg)were divided into two groups. The left eyes of rabbits underwent standard glaucoma trabecular resection were treatment group, and the normal right eyes served as controls. Transparency of lenses was monitored by a slit-lamp biomicroscopy before and after glaucoma trabecular resection. The morphology of lens cells was observed under the light microscope.The activities of Na+-K+-ATPase,catalase(CAT), glutathion peroxidase(GSH-px), glutathione reductase(GR), superoxide dismutase(SOD)and content of malondialdehyde(MDA)in lenses were detected six months after trabecular resection.
RESULTS: Lenses were clear in both treatment group and normal control group during the six months after operation. The morphology and structure of lens cells were normal under the light microscope in both operation group and normal group. The activity of lens cells antioxidant enzyme activity were significantly decreased in operation group compared with control group, Na+-K+-ATPase declined by 20.97%, CAT declined by 16.36%, SOD declined by 4.46%, GR declined by 4.85%, GSH-px declined by 10.02%, and MDA increased by 16.31%.
CONCLUSION: Glaucoma trabecular resection can induce the change of Na+-K+-ATPase, CAT, GSH-px, GR, SOD and MDA in lens of rabbit. Glaucoma filtration surgery for the occurrence of cataract development mechanism has important guiding significance.
[中图分类号]
[基金项目]
陕西省科学技术研究发展计划项目(No.2012K16-11-03)