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目的:已有一些临床试验和基础研究显示灯盏细辛(GerigeronBreviscapus(vant)Hand-Maz2EBHM),对青光眼患者及动物模型有神经保护的作用,本研究探讨灯盏细辛是否对NMDA导致的大鼠RGCL神经元兴奋毒性有保护作用。方法:60只健康SD大鼠随机分为4组,其中6只为正常对照组(A组),其余54只随机分为3组,分别为B组(EBHM组),C组(生理盐水+NMDA组),D组(EBHM+NMDA组),每组各18只大鼠。C、D两组大鼠右眼玻璃体内注射NMDA10nmol/2μL制成视网膜损伤模型,左眼玻璃体内注射相同剂量PBS液作为自身对照。B组及D组均在NMDA注射前7d起按150mg/(kg·d)日剂量予60g/LEBHM腹腔内注射,C组予生理盐水0.5mL腹腔内注射。在NMDA处理后4,7,14d处死动物剥取视网膜作全层铺片行RGCL神经元计数分析。结果:正常对照组双眼RGCL神经元计数比较差异无显著性意义(P=0.200)。NMDA干预后4,7,14dEBHM组RGCL神经元计数,双眼与正常对照组比较差异无显著性意义(P>0.05)。生理盐水+NMDA及EBHM+NMDA组实验眼在以上各时段RGCL神经元计数与正常组比较差异均有非常显著性意义(P<0.001),左眼与正常对照组比较差异无显著性意义(P>0.05)。实验眼14d时RGCL神经元计数EBHM+NMDA组高于生理盐水+NMDA组,二者比较差异有显著性(P=0.044),但仍低于正常对照组(P<0.05)。结论:单独使用EBHM对正常大鼠RGCL神经元计数无影响,EBHM可对NMDA所致大鼠RGCL神经毒性提供部分保护作用。
OBJECTIVE: There have been some clinical trials and basic studies that have shown that Ginger Breviscapus (vant) Hand-Maz2EBHM has neuroprotective effects on glaucoma patients and animal models. This study investigated whether Erigeron Breviscapus causes NMDA-induced rat RGCL. Neuronal excitotoxicity has a protective effect. METHODS: Sixty healthy Sprague-Dawley rats were randomly divided into 4 groups. Six of them were normal controls (group A), and the remaining 54 were randomly divided into 3 groups: group B (EBHM group) and group C (normal saline + NMDA group), D group (EBHM+NMDA group), 18 rats in each group. The retinal injury model was induced by intravitreal injection of NMDA 10 nmol/2 μL in the right eye of groups C and D, and the same dose of PBS was intravitreally injected into the left eye as the autologous control. Both groups B and D were injected intraperitoneally with 60g/LEBHM daily for 150mg/(kg·d) from the 7th day before NMDA injection. In group C, 0.5mL normal saline was intraperitoneally injected. After 4 days, 7 days and 14 days after NMDA treatment, the animals were sacrificed and the retina was completely covered with RGCL neurons. Results: There was no significant difference in the number of RGCL neurons in the normal control group (P=0.200). There were no significant differences in the number of RGCL neurons in the EBHM group between the 4th, 7th and 14th day after NMDA intervention (P>0.05). In the normal saline, NMDA, and EBHM+NMDA groups, the difference between the RGCL neuron counts and the normal group at each time point was significant (P<0.001). There was no significant difference between the left eye and the normal control group (P<0.001). >0.05). The number of RGCL neurons at the 14th day of the experimental day was higher in EBHM+NMDA group than in saline+NMDA group, and the difference between the two groups was significant (P=0.044), but still lower than that in the normal control group (P<0.05). CONCLUSION: EBHM alone has no effect on the number of RGCL neurons in normal rats. EBHM may provide partial protection against NRG-induced RGCL neurotoxicity.