刺五加联合尼莫地平对兔慢性青光眼视网膜损伤的保护作用

目的探讨中药刺五加和钙通道阻滞剂尼莫地平对青光眼视网膜神经节细胞的保护作用及其作用机理。方法用前房注射2.5%羟丙基甲基纤维素的方法建立日本大耳白兔双眼实验性慢性青光眼模型。动态观察眼压,高眼压维持4周后行双眼小梁切除术。实验兔随机分为刺五加组、尼莫地平组、联合用药组和空白对照组,分别喂服上述药物。于前房注射前、注射后4、8、12周抽取双眼玻璃体,利用高效液相色谱分析检测玻璃体谷氨酸浓度。结果各组间前房注射前后、小梁切除术后眼压差异均无显著性(P>0.05)。前房注射前4组间玻璃体谷氨酸浓度差异无显著性(P>0.05),前房注射后4、8、12周,各组玻璃体谷氨酸浓度均高于注射前(P<0.01)。刺五加组、尼莫地平组、联合用药组玻璃体谷氨酸浓度低于对照组(P<0.05)。结论慢性实验性青光眼兔眼玻璃体谷氨酸浓度明显升高;刺五加和尼莫地平通过抑制玻璃体谷氨酸浓度的升高起到保护青光眼兔眼视神经保护的作用。

The neuroprotective effect of acanthopanax senticocus and nimodipine on RGCs in rabbit eyes with chronic glaucoma

OBJECTIVE To study the neuroprotective effect of Acanthopanax senticosus(AS)and nimodipine on glaucomatous Retinal Ganglion Cells(RGCs).METHODS The rabbit models of experimental chronic glaucoma were produced by injecting 2.5 % methylcellulose into bilateral anterior chamber.Chronic,moderately elevated intraocular pressure(IOP)lasted for 4 weeks and then decreased by trabeculectomy.The rabbits were divided into AS group,nimodipine group,united group and control group.The medicine was given orally and respectively after trabeculectomy.Vitreous glutamate concentration of those rabbits in each group was analysed by means of high-performance liquid chromatography before injection and at 4,8,12 weeks post-injection.One rabbit sacrificed at the 4th week was used for histopathological examination.RESULTS There was no significant difference between IOP of AS group,nimodipine group,united group and control group pre-injection,post-injection or post-trabeculectomy.Nerve fiber layer,ganglion cell layer and inner nuclear layer were damaged in experimental chronic glaucomatous eyes.RGCs died with a trait of apoptosis.Before injection,there was no significant difference among the vitreous glutamate concentrations of AS group,nimodipine group,united group and control group(P>0.05).At 4,8 and 12 week,the vitreous glutamate concentration of AS group,nimodipine group and united group was significantly lower than control group(P<0.05).CONCLUSIONS Vitreous glutamate concentration in experimental glaucomatous eye was elevated significantly.Both AS and nimodipine could protect RGCs from damage induced by experimental glaucoma in rabbit.Inhibiting the elevation of vitreous glutamate concentration is the possible mechanism.