Wang Lianfeng, Cao Tingting, Chen Haiting
Section One, Department of Ophthalmology, Cangzhou Central Hospital, Cangzhou, Hebei 061001, P.R. China.
Exp Ther Med. 2018 Jan;15(1):300-304. doi: 10.3892/etm.2017.5386. Epub 2017 Oct 27.
The treatment of glaucomatous optic nervedamage using ginsenoside Rg1 mediated by ultrasound targeted microbubbles destruction was evaluated. Thirty healthy New Zealand white rabbits were subjected to injection of 0.3% carbomer solution to establish glaucomatous optic nerve damage model. Rabbits were divided into 5 groups: control group, model group, model group + intravitreal injection of nerve growth factor (NGF) group, model group + intravitreal injection of ginsenoside Rg1 group (Rg1 group), model group + intravitreal injection of ginsenoside Rg1 + ultrasound microbubble group (ultrasound group), model group + ultrasound targeted microbubble destruction (ultrasound group). Intraocular pressures were compared at 1, 2 and 4 weeks after model establishment. Rabbits were sacrificed 4 weeks after model establishment to collect retinal tissue for H&E staining. Histological changes were observed and the retinal thickness was measured. Contents of malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide (NO) were measured by ELISA. Intraocular pressure was significantly higher in model group than in control group at 1 week (P<0.05). Intraocular pressure was significantly lower in the ultrasound group than in NGF group and Rg1 group at all time-points (P<0.05). The number of ganglion cells in model group was decreased significantly. Number of nuclear layer cells was significantly reduced. Thickest retina was found in control group and model group was the thinnest (P<0.05). Contents of MDA and NO in model group were significantly higher than those in NCF group and Rg1 group. SOD content in control group was higher than that in ultrasound group and model group (P<0.05). In conclusion, treatment of glaucomatous optic nerve damage using ginsenoside Rg1 mediated by ultrasound targeted microbubble destruction can reduce the level of oxidative stress, relieve intraocular pressure and reduce ganglion cell damage.
评估了超声靶向微泡破坏介导人参皂苷Rg1治疗青光眼性视神经损伤的效果。将30只健康的新西兰白兔注射0.3%卡波姆溶液以建立青光眼性视神经损伤模型。将兔子分为5组：对照组、模型组、模型组+玻璃体内注射神经生长因子（NGF）组、模型组+玻璃体内注射人参皂苷Rg1组（Rg1组）、模型组+玻璃体内注射人参皂苷Rg1+超声微泡组（超声组）、模型组+超声靶向微泡破坏组（超声组）。在模型建立后1、2和4周比较眼压。在模型建立后4周处死兔子，收集视网膜组织进行苏木精-伊红染色。观察组织学变化并测量视网膜厚度。通过酶联免疫吸附测定法测量丙二醛（MDA）、超氧化物歧化酶（SOD）和一氧化氮（NO）的含量。模型组在1周时眼压显著高于对照组（P<0.05）。超声组在所有时间点眼压均显著低于NGF组和Rg1组（P<0.05）。模型组神经节细胞数量显著减少。核层细胞数量显著减少。对照组视网膜最厚，模型组最薄（P<0.05）。模型组MDA和NO含量显著高于NCF组和Rg1组。对照组SOD含量高于超声组和模型组（P<0.05）。总之，超声靶向微泡破坏介导人参皂苷Rg1治疗青光眼性视神经损伤可降低氧化应激水平，缓解眼压并减少神经节细胞损伤。
