EGCG脂质体抑制大鼠角膜新生血管的研究

来源 :中国急救复苏与灾害医学杂志 | 被引量 : 0次 | 上传用户:chi421
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目的 研究表没食子儿茶素没食子酸酯(Epigallocatechin-3-gallate,EGCG)脂质体对大鼠角膜新生血管的抑制作用.方法 采用逆相蒸发法制备EGCG脂质体,测定粒径、Zeta电位.实验鼠随机分为生理盐水组、空白脂质体组、地塞米松组和EGCG脂质体组.建立角膜新生血管模型并给予相应药物治疗.裂隙灯观察角膜炎症反应、角膜混浊程度和角膜新生血管生长情况.HE染色观察角膜形态变化.正常大鼠结膜下注射EGCG脂质体,评价其对大鼠眼有无明显毒性.结果 EGCG脂质体组粒径为(81.96±3.46)nm,Zeta电位为(-31.8±0.44)mV.烧伤后第3、7、14d,EGCG脂质体组和地塞米松组炎症指数分别为(4.25±0.46)分和(3.63±0.52)分;(3.38±0.74)分和(2.63±0.52)分;(2±0.53)分和(2.13±0.64)分,与生理盐水组相比,炎症指数下降(P<0.05).烧伤后第3、7、14d,EGCG脂质体组和地塞米松组角膜混浊评分分别为(3.13±0.64)分和(3±0.76)分;(2.19±0.83)分和(2.13±0.64)分;(2±0.76)分和(2.13±0.64)分,与生理盐水组相比,角膜混浊减轻(P<0.05).烧伤后第3、7、14d,EGCG脂质体组和地塞米松组新生血管面积分别为(6±0.46)mm2和(5.23±0.22)mm2;(14.06±1.19)mm2和(11.61±1.49)mm2;(21.56±3.56)mm2和(20.3±3)mm2,与生理盐水组相比,角膜新生血管面积减少(P0.05);病理切片示角膜无炎性细胞浸润.结论 EGCG脂质体安全性好,减轻角膜炎症,抑制角膜新生血管生长.EGCG脂质体有望成为治疗角膜新生血管类疾病的新型眼用制剂,为其治疗提供新思路.“,”Objective To investigate the inhibiting effect of epigallocatechin-3-gallate liposomes on corneal neovascularization (CNV) of rats. Methods Epigallocatechin-3-gallate liposomes were prepared by reverse-phase evaporation. The particle size and zeta potential were determined. Rats were randomLy divided into 4 groups, physiological saline group, blank liposomes group, dexamethasone group and epigallocatechin-3-gallate liposomes group. The alkali burn induced corneal neovascularization models were built and respectively processed with the above medicines. The level of corneal inflammation reaction, corneal opacity, and the growth of corneal neovascularization were analyzed by the slit-lamp microscopy. Tissue sections were stained with histological examination to observe the morphology of the corneas. Epigallocatechin-3-gallate liposomes were injected into the eyes of the normal rats. The toxicity of epigallocatechin-3-gallate liposomes were observed by praxiology,slit-lamp biomicroscope. Pathological specimens were made to observe the differences under a light microscope at the 14th day after using medication. Results The particle size was (81.96 ± 3.46) nm and the average zeta potential was (-31.8 ± 0.44) mV. At the third day, 7th day, 14th day, the level of corneal inflammation reaction of epigallocatechin-3-gallate liposomes group and dexamethasone group were (4.25 ± 0.46) scores and (3.63 ± 0.52) scores;(3.38 ± 0.74) scores and (2.63 ± 0.52) scores;(2 ± 0.53) scores and(2.13 ± 0.64)scores , compared with physiological saline group, the corneal inflammation reaction were effectively inhibited (P<0.05). At the third day, 7th day, 14th day, the corneal opacity of epigallocatechin-3-gallate liposomes group and dexamethasone group were (3.13 ± 0.64)scores and (3 ± 0.76) scores;(2.19 ± 0.83) scores and (2.13 ± 0.64) scores;(2 ± 0.76) scores and(2.13 ± 0.64)scores , compared with the physiological saline group, the corneal opacity were effectively inhibited (P<0.05). At the third day, 7th day, 14th day, the growth of corneal neovascularization of epigallocatechin-3-gallate liposomes group and dexamethasone group were (6 ± 0.46) mm2 and (5.23±0.22) mm2;( 14.06±1.19) mm2 and (11.61±1.49) mm2;( 21.56±3.56) mm2 and(20.3±3)mm2,compared with physiological saline group, the growth of corneal neovascularization were effectively inhibited (P0.05). The corneal histological structure was without the infiltration of inflammatory cell in all corneas. Conclusion The safety of the epigallocatechin-3-gallate liposomes were relatively good. Epigallocatechin-3-gallate liposomes could reduce inflammation reaction and inhibit the growth of corneal neovascularization. Epigallocatechin-3-gallate liposomes are novel ophthalmic delivery formulations for the treatment of corneal neovascularization, which provide a new idea for the treatment of corneal neovascularization.
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