TMB-8体外对神经细胞保护作用及其机理的研究
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Protective Effects and Mechanism of TMB-8 on Neuron
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    摘要:

    研究TMB-8[8-(N,N-二乙胺)-n-辛基-3,4,5-三甲氧基苯甲酸酯]的神经保护作用及其可能机制。方法 用氧-葡萄糖剥夺模型观察TMB-8对培养的大鼠神经细胞形态、细胞膜通透性和细胞内丙二醛(MDA)、总过氧化物歧化酶(TSOD)、谷胱甘肽(GSH)和谷胱甘肽过氧化物酶(GSH-PX)的影响, 结果 经氧—葡萄糖剥夺1h后.无血清培养24h的神经细胞 乳酸脱氢酶(LDH)漏出明显增加,细胞内GSH的含量和T-SOD的活性显著降低,TMB-8能剂量依赖性地减少LDH的漏出,能 升高细胞内GSH和提高细胞内T-SOD的活性。结论 TMB-8的神经保护作用可能与增加神经细胞内GSH的水平和提高TSOD的活性有关。

    Abstract:

    To investigate the neuroprotective effect and mechanism of TMB 8[8- (N, N-diethy lamino)- n -octyl- 3,4,5- trimethoxybenzoate]. Methods The oxygen-glucose deprivation model of cultured rat neu ron was used to observe the effects of TMB-8 on neuron morphology, permeability and contents of MDA, GSH, TSOD and GSH px in neurons. Results The damaged neurons induced by oxygen glucose deprivation for 1 h and after serum-free culture for 24 h could liberate much LDH; the contents of GSH and the activity of T SOD in neurons were significantly decreased; TMB-8 could concentration dependently reduce the efflux of LDH from the damaged neuron and increase the content of GSH in neuron, the activity of T-SOD in these cells was also increased. Conclusion the neuroprotective role of TMB-8 may be related to the increasing of GSH and T SOD in the damaged neuron.

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肖继皋,王斌,徐昌盛. TMB-8体外对神经细胞保护作用及其机理的研究[J].南京医科大学学报(自然科学版),2000,20(03):

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