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Neuroprotective effects of an extract from the inflamed skin of rabbits inoculated with vaccinia virus on glutamate-induced neurotoxicity in cultured neuronal cell line

机译:接种痘苗病毒的兔子发炎皮肤提取物对谷氨酸诱导的神经元细胞系神经毒性的保护作用

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Objective: Protein-free extracts from the inflamed skin of rabbits inoculated with vaccinia virusn(RosemorgenH and NeurotropinH) are widely employed to combat chronic pain and treat allergicnconditions in human subjects in Japan. However, the pharmacologic mechanisms ofnRosemorgenH and NeurotropinH remain unclear.nMethods: In this study, we examined the effects of RosemorgenH on L-glutamic acid (Glu)-ninduced cell death in N18-RE-105 neural cell line, which only possessed non-N-methyl-Daspartaten(NMDA)-type receptors.nResults: There were many large cytoplasmic cells and elongation of fivers in phosphate-bufferednsaline (PBS) additional group without Glu. In PBS and Glu simultaneous additional group, thensurvival ratio was decrease significantly compared with PBS alone group. Moreover, there werendead cells which did not have cytoplasm and aggregated nucleus. The Glu-induced cell death ofnN18-RE-105 cells was inhibited by both pre-treatment (24 hours before Glu treatment) andnsimultaneous treatment with RosemorgenH. There were many large cytoplasmic cells andnelongation of fivers in RosemorgenH group.nDiscussion: From this finding in N18-RE-105 cells, RosemorgenH was concluded to inhibit Gluinducedncell death via non-NMDA type receptors. One of the pharmacologic mechanisms ofnRosemorgenH has been clear. These results suggest that RosemorgenH depresses allodynia and chronicnpain through interaction with non-NMDA type receptors. [Neurol Res 2008; 30: 430–434]
机译:目的:接种痘苗病毒(RosemorgenH和NeurotropinH)的兔子发炎皮肤中的无蛋白提取物被广泛用于抗击慢性疼痛并治疗日本人的过敏性疾病。然而,nRosemorgenH和NeurotropinH的药理机制仍不清楚。结果:没有Glu的磷酸缓冲盐碱(PBS)附加组中有许多大的细胞质细胞,并且延伸了firs。 PBS和Glu同时追加组的生存率明显低于PBS组。此外,还存在没有细胞质和聚集核的死细胞。预处理(Glu处理前24小时)和同时用RosemorgenH处理均抑制了Glu诱导的nN18-RE-105细胞的细胞死亡。讨论:从N18-RE-105细胞中发现,罗斯莫根H被认为可以通过非NMDA型受体抑制Glu诱导的细胞死亡。 nRosemorgenH的药理机制之一已经很清楚。这些结果表明,RosemorgenH通过与非NMDA型受体相互作用来抑制异常性疼痛和慢性痛。 [Neurol Res 2008; 30:430–434]

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