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目的:探讨大鼠视神经损伤后远志皂苷元干预对损伤视神经及视网膜神经节的影响及机制。方法:SPF级雌性SD大鼠65只,随机取20只大鼠为正常组,不予任何处理。余45只行视神经钳夹法造模(右眼),5只大鼠造模失败,予以剔除,余40只纳入实验。将其随机分为:视神经损伤组和远志皂苷元组,各20只/组。视神经损伤组大鼠无治疗,常规饲养,远志皂苷元组大鼠予以远志皂苷元治疗。造模后4 d,各实验组大鼠视网膜和视神经细胞以TUNEL法检测细胞凋亡,造模后7 d,RT-PCR、Western blot行大鼠视网膜和视神经节细胞组织Bax、Bcl-2基因和蛋白表达检测。造模后14 d,行闪光视觉诱发电位检测。最后处死大鼠取眼球,观察各组大鼠视网膜和视神经的病理形态,行视网膜神经节细胞计数。结果:造模后4 d,远志皂苷元组视网膜神经节细胞凋亡数量明显低于视神经损伤组(P<0.05),造模后7 d与视神经损伤组相比远志皂苷元组Bax基因和蛋白表达显著降低P<0.05);Bcl-2基因和蛋白表达显著升高P<0.05)。造模后14 d,荧光金阳性RGC数:视神经损伤组最少,远志皂苷元组较多,正常组最多,且各组之间差异有统计学意义(P<0.05)。远志皂苷元组大鼠闪光视觉诱发电位伏期较视神经损伤组大鼠短(P<0.05)、波幅明显高于视神经损伤组(P<0.05)。结论:远志皂苷元干预通过减少大鼠视神经钳夹后RGCs的凋亡,降低视网膜Bax基因和蛋白的表达,促进BCL-2基因基因和蛋白的表达,对视神经损伤起到保护作用。
Objective: To investigate the effect and mechanism of teigenin on the injured optic nerve and retinal ganglion after optic nerve injury in rats. Methods: A total of 65 SPF female SD rats were randomly divided into normal group and 20 rats without any treatment. More than 45 optic nerve clamp model (right eye), 5 rats failed to model, to be removed, the remaining 40 were included in the experiment. They were randomly divided into: optic nerve injury group and teigenin group, each 20 / group. Rats in optic nerve injury group were given no treatment and routinely fed. The rats in Polygalaceae saponin group were given Polygala sapogenin. At 4 days after model establishment, retinal and optic nerve cells in each experimental group were assayed for apoptosis by TUNEL method. Seven days after model establishment, Bax and Bcl-2 genes were detected by RT-PCR and Western blot in rat retinas and optic ganglion cells And protein expression detection. Fourteen days after modeling, flash visual evoked potentials were measured. Finally, the rats were sacrificed to take the eyeball, the retina and optic nerve in each group were observed pathological morphology, retinal ganglion cell count. Results: At 4 days after modeling, the number of retinal ganglion cell apoptosis in the group treated with teicopinin was significantly lower than that in the group with optic nerve injury (P <0.05). Compared with the optic nerve injury group, the levels of Bax gene and protein P <0.05), while the expression of Bcl-2 gene and protein was significantly increased (P <0.05). Fourteen days after modeling, the number of RGCs positive for fluorescent gold was the lowest in optic nerve injury group, the more in saporin saponin group, the most in normal group, and the difference was statistically significant (P <0.05). Compared with the rats with optic nerve injury, the amplitude of visual evoked potentials in the group treated with tenebrio saponin was shorter (P <0.05), and the amplitude was significantly higher than that in optic nerve injury group (P <0.05). CONCLUSION: Polygala root sapogenin can protect the optic nerve injury by decreasing the apoptosis of retinal ganglion cells, decreasing the expression of Bax gene and protein in retina, and promoting the gene and protein expression of BCL-2 gene.