氨基胍对大鼠慢性高眼压视网膜PI-3K表达的影响

目的研究慢性高眼压过程中大鼠视网膜磷脂酰肌醇-3-激酶（PI-3K）表达的变化及应用氨基胍对其表达的影响，探讨氨基胍对慢性高眼压视网膜的保护作用。方法应用免疫组织化学、RT-PCR和Westernblot的方法，观察应用及未应用氨基胍的慢性高眼压大鼠视网膜在不同时点的差异及PI-3K表达的变化。结果与正常对照组相比，慢性高眼压大鼠应用与未应用氨基胍者，视网膜均随着高眼压时间的延长逐渐出现形态学变化，于高眼压的第21d视网膜变薄，节细胞数量减少；在此过程中，PI-3K表达增多。慢性高眼压大鼠的视网膜应用氨基胍者与未应用氨基胍者相比，其形态学变化较小，而PI-3K表达则明显增多，两者差异具有统计学意义（P〈0．01）。结论PI-3K是慢性高眼压视网膜损伤过程中的保护性因素，氨基胍通过上调其表达发挥对视网膜的保护作用。

Influence of amino-guanidine on the expression of PI-3K in retina of rats with chronic IOP elevation

Objective Research showed that amino-guanidine （AG） has a pretection effect on optical nerve. But its action and mechanism on chronic hypertention are not understood well. This paper was to study the change of phosphatidylinositol-3- kinase （PI-3K） expression in rat retina and the effect of AG on the course of chronic intraoeular pressure（IOP） elevation. Methods Fifty Wistar rats were divided into blank control group（ 10 rats） ,chronic hypertension group（30 rats） and AG group （30 rats）. Chronic hypertention was created by cauterizing the superficial scleral veins. 150 mg/（ kg ·d） AG was given by oral 1 day before cauterization. Immunohistochemistry, RT-PCR and Western blotting were used respectively to observe the changes of expression of PI-3K in the model rats and AG interference rats at different time points during the course of chronic IOP elevation. Results The successful model was identified as the IOP over 40% of normal rats. The retinal thickness was significantly reduced in model group and model ＋ AG group compared with normal rats from 21 days through 28 days after cauterization（ P 〈 0. 05 ） , and that of model rats was obviously decreased in comparison with model ＋ AG rats （ P 〈 0.05 ）. The number of ganglion cells was significantly decreased in model rats and model ＋ AG rats compared with normal rats from 21 days to 28 days. The stronger IOD value was seen for PI-3K in the model ＋ AG rats by immunochemistry（P 〈 0.01 ）, and the expressions of PI-3K mRNA and protein were considerably increased in model ＋ AG rats compared with model rats by RT-PCR and Western blotting respectively（ P 〈 0.05 -0.01 ）. Conclusion AG has a protective effect on retinal damage caused by chronic IOP elevation. This goal is achieved by regulating the expression of PI-3K,a protective factor of hypertensive-injury,in retina.