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目的:研究银杏内脂B微乳油剂对视网膜神经节细胞的保护作用,探讨其可能的作用机制,从而为其治疗青光眼等视网膜相关疾病提供理论依据。方法:选取出生后46 d的SD大鼠30只;随机抽取10只为A组(正常对照组);余下20只建立青光眼大鼠模型,按照SD大鼠体重1次腹腔注射60 mg/kg N-甲基-N-亚硝脲建立青光眼大鼠模型,并分为两组即B组(模型对照组)和C组(银杏内酯B治疗组),每组10只;A组不做任何处理,C组SD大鼠在实验前7 d每日腹腔注射银杏内酯B微乳油剂40 mg/kg;B组SD大鼠给等量生理盐水灌胃;实验1周、2周后分别行闪光视觉诱发电位及视网膜形态学分析测量中心视网膜外层厚度。结果:实验1周后,正常对照组、模型对照组、银杏内酯B治疗组的LP1和AP1分别为[(91±3)ms,(18±4)μV]、[(110±4)ms,(13±4)μV]、[(95±3)ms,(17±3)μV],银杏内酯B治疗组与正常对照组、模型对照组存在显著性差异,差异有统计学意义(P<0.05)。实验后2周,形态学检查结果表明正常对照组大鼠的中心视网膜外层厚度为(97.4±1.6)μm,模型对照组外视网膜厚度为(16.8±2.1)μm,而银杏内酯B治疗组外视网膜厚度为(24.2±2.3)μm,模型对照组与银杏内酯B治疗组均明显高于正常对照组,差异有统计学意义(P<0.05);而银杏内酯B治疗组显著高于模型对照组,差异有统计学意义(P<0.05)。结论:银杏内脂B微乳油剂对N-甲基-N-亚硝脲所致青光眼大鼠的视网膜神经细胞具有一定的保护作用,其可能的机制在于银杏内脂B通过调节青光眼大鼠的动作电位,同时修复损伤的视网膜,从而发挥视网膜保护作用。本研究对银杏内脂B微乳油剂视网膜神经节细胞的保护作用,并揭示了其作用机制,对银杏内脂B微乳油剂在青光眼等视网膜相关疾病的治疗提供了重要的理论基础。
OBJECTIVE: To study the protective effect of ginkgolide B microemulsion on retinal ganglion cells and to explore its possible mechanism of action, thus providing a theoretical basis for the treatment of retinal related diseases such as glaucoma. Methods: Thirty SD rats were selected at 46 days after birth. Ten rats were randomly selected as group A (normal control group). The remaining 20 rats were established by intraperitoneal injection of 60 mg / kg N - methyl-N-nitrosourea to establish a rat model of glaucoma and divided into two groups that is B group (model control group) and C group (Ginkgolide B treatment group), each group of 10; A group without any The rats in Group C were injected intraperitoneally with Ginkgolide B microemulsion 40 mg / kg on the 7th day before the experiment. The rats in Group B were given the same amount of saline for gavage. One week and two weeks later, Flash visual evoked potentials and retinal morphology analysis of the central retinal thickness. Results: After 1 week of experiment, LP1 and AP1 in the normal control group, model control group and ginkgolide B treatment group were (91 ± 3) ms, (18 ± 4) μV] and [110 ± 4) ms , (13 ± 4) μV], [(95 ± 3) ms, (17 ± 3) μV] respectively. There was a significant difference between Ginkgolide B treatment group and normal control group and model control group P <0.05). Morphological examination results showed that the thickness of the central retinal layer in the normal control group was (97.4 ± 1.6) μm and the retinal thickness in the model control group was (16.8 ± 2.1) μm two weeks after the experiment, while the ginkgolide B treatment group The thickness of the outer retina was (24.2 ± 2.3) μm, the model control group and ginkgolide B treatment group were significantly higher than the normal control group, the difference was statistically significant (P <0.05); while ginkgolide B treatment group was significantly higher The model control group, the difference was statistically significant (P <0.05). CONCLUSION: Ginkgolide B microemulsion has a protective effect on retinal neurons in glaucomatous rats induced by N-methyl-N-nitrosourea. The possible mechanism is that ginkgolide B can regulate retinal neurons in glaucoma rats Action potential, while repairing damaged retina, which play a role in retinal protection. In this study, the protective effect of ginkgolide B microemulsion on retinal ganglion cells was studied and its mechanism of action was revealed. This study provides an important theoretical basis for the treatment of retinal ganglion-related diseases such as glaucoma by ginkgolide B microemulsion.