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灯盏细辛对NMDA所致的大鼠视网膜神经元损伤的保护作用
引用本文:石晶明,蒋幼芹,刘旭阳.灯盏细辛对NMDA所致的大鼠视网膜神经元损伤的保护作用[J].眼科学报,2004,20(2):113-117.
作者姓名:石晶明  蒋幼芹  刘旭阳
作者单位:1. 中山大学湘雅第二医院,长沙,410011
2. 美国威斯康辛大学医学院眼科
摘    要:目的:探讨灯盏细辛(EBHM)是否对N-甲基-D天门冬氨酸(NMDA)导致的大鼠视网膜神经节细胞层(RGCL)神经元兴奋毒性损伤有保护作用。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(生理盐水加NMDA组),D组(EBHM加NMDA组),每组各18只大鼠。C、D两组大鼠右眼玻璃体内注射NMDA 10 nmol/2 μl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15 mg·100 g-1·d-1剂量予6%EBHM腹腔内注射,C组予生理盐水0.5 ml腹腔内注射。在NMDA处理后4,7和14 d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 d和14 dEBHM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)。生理盐水加NMDA及EBHM加NMDA组实验眼在以上各时段RGCL神经元计数与正常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14 d时RGCL神经元计数EBHM加NMDA组高于生理盐水加NMDA组,两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N

关 键 词:灯盏细辛  NMDA  视网膜  大鼠  神经元损伤  神经保护  青光眼

Neuroprotective Effect of Erigeron Breviscapus (vant) Hand-Mazz on NMDA-induced Retinal Neuron Injury in the Rats
Jingming Shi,Youqinjiag,Xuyang Liu.Neuroprotective Effect of Erigeron Breviscapus (vant) Hand-Mazz on NMDA-induced Retinal Neuron Injury in the Rats[J].Eye Science,2004,20(2):113-117.
Authors:Jingming Shi  Youqinjiag  Xuyang Liu
Institution:Department of Ophthalmology, The Second Xiangya Hospital of Central South University, Changsha 410011, China. sjm93cn@yahoo.com.cn
Abstract:PURPOSE: To investigate if Erigeron Breviscapus (vant) Hand-Mazz (EBHM) has a neuroprotective effect against NMDA-induced neuron death in retinal ganglion cell layer (RGCL). METHODS: Sixty healthy SD rats were randomly divided into four groups. 6 animals were in normal control group (group A). The others were divided as group B (EBHM group), group C (normal saline+NMDA group), group D (EBHM+NMDA group). Each group has 18 rats. 10 nmol NMDA was chosen for intravitreal injection to cause partial damage of the neurons in RGCL in the right eyes of Groups C and D. Same volume PBS was intravitreal injected in the left eyes as self-control. Groups B and D were pre-treated intraperitoneally with 6% EBHM solution at a dose of 15 mg x 100 g(-1) x d(-1) seven days before and after NMDA treatment. Group C were administrated intraperitoneally with 0.9% normal saline at the same time of EBHM injection. Rats were sacrificed in 4, 7, 14 days after NMDA treatment. Flat preparation of whole retinas were stained with 0.5% cresyl violet and neuron counting in RGCL from both eyes. Each subgroup has 6 rats. RESULTS: There was no significant difference between the right eye and the left eye of neuron counting from RGCL in normal control group (group A) (P=0.200). There was no significant difference between normal control group and EBHM group either in the right eyes or in the left eye in 4 days, 7 days and 14 days respectively after intravitreal injection of 10 nmol NMDA in group C and group D. (P=0.636, P=0.193). Neuron counting from RGCL of group C and group D were significant decreased in the NMDA-treated eyes in 4 days, 7 days and 14 days after intravitreal injection (P < 0.001). There ws no significant difference between self-control eyes and normal control group (P > 0.05). Neuron counting was significantly higher in the EBHM+NMDA group than normal saline+NMDA group at 14 days after intraviteal injection (P=0.044). However,it is obvious that the difference was still significant between normal control group and EBHM+NMDA group (P < 0.05). CONCLUSION: EBHM has no effect on neuron counting of RGCL when administered alone in normal rats. It is suggested that EBHM has partial protective effect on NMDA-induced neuron loss in RGCL in the rat.
Keywords:excitatory amino acids  glaucoma  neuroprotection  erigeron breviscapus (vant) hand-mazz
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