对氨基水杨酸钠对锰致大鼠基底核神经元损伤影响的体外研究

发布时间：2018-05-05 16:33

本文选题：锰 + 对氨基水杨酸钠　；参考：《广西医科大学》2013年硕士论文

【摘要】：目的探讨对氨基水杨酸钠(PAS-Na)对体外锰致大鼠原代基底核神经元损伤的影响。材料与方法培养至第8天的基底核神经元随机分为正常对照组(对照组)、低、中、高剂量染锰(L-、M-、H-Mn)组、PAS-Na (PAS)对照组、低、中、高剂量PAS-Na (L-、M-、H-PAS)干预组。对照组神经元给予培养液培养24h；染锰组神经元暴露于MnCl2·4H2O100、200、400μ mol/L培养液培养24h; PAS对照组神经元给予含PAS-Na50、500、5000μ mol/L培养液培养24h。L-、M-、H-PAS干预组神经元分别暴露于MnCl2·4H2O100、200、400μ mol/L培养液培养24h,接着弃掉原培养液,再分别给予含PAS-Na50、500、5000μ mol/L的培养液培养24h。其余组培养液培养24h。然后,用噻唑蓝(MTT)法测定存活率,单细胞凝胶电泳技术(SCGE)测定DNA损伤,硫代巴比妥酸(TBA)测定丙二醛(MDA),水溶性四唑盐(WST-1)法测定测定超氧化物歧化酶(SOD)活力。结果(1)锰可引起基底核神经元形态损伤和存活率呈剂量-反应性下降。(2)PAS-Na对基底核神经元形态无明显影响,各PAS-Na剂量组的存活率与对照组有差异,但组间无剂量-反应关系。(3)与对照组相比,染锰组神经元存活率明显降低,彗星尾部DNA百分率、Olive尾距增高,MDA含量增加,SOD活力下降,差异有统计学意义(P0.05)。(4) L-、M-PAS干预使暴露于L-Mn组神经元存活率提高,彗星尾部DNA百分率、Olive尾距降低,MDA含量减少,SOD活力增高,差异有统计学意义(P0.05)。(5)M-PAS干预使暴露于M-Mn组神经元存活率提高,彗星尾部DNA百分率、Olive尾距降低,SOD活力增高,差异有统计学意义(P0.05)。结论体外染锰对大鼠原代基底核神经元损伤明显,PAS-Na对锰致基底核神经元毒性有一定的干预作用。
[Abstract]:Objective to investigate the effect of sodium p aminosalicylate (PAS-Na) on primary basal nucleus neuron injury induced by manganese in vitro in rats. Materials and methods the neurons of basal nucleus cultured to the 8th day were randomly divided into normal control group (control group, low, medium, high dose manganese-exposed group) control group (PAS-Na PAS-PAS-PAS-PAS-PAS-PAS-PAS-PAS-PAS-PAS-PAS-treated group), low-dose, moderate-dose, high-dose PAS-Na group (control group). Neurons in control group were cultured in culture medium for 24 h, neurons in manganese group were exposed to MnCl2 4H2O100200400 渭 mol/L for 24 h, neurons in PAS control group were exposed to MnCl2 4H2O100200400 渭 mol/L medium for 24 h, and those in PAS control group were exposed to MnCl2 4H2O100200400 渭 mol/L medium for 24 h. The culture medium containing PAS-Na 50500 渭 mol/L was cultured for 24 h. The other groups were cultured in culture medium for 24 hours. Then, the survival rate was determined by thiazolyl blue, DNA damage was detected by single cell gel electrophoresis, malondialdehyde (MDA) was measured by thiobarbituric acid (TBA), and the activity of superoxide dismutase (SOD) was determined by water-soluble tetrazolium salt (WST-1). Results (1) Manganese could induce the morphological damage and survival rate of basal nucleus neurons decreased dose-reactively. PAS-Na had no significant effect on the morphology of basal nucleus neurons. The survival rate of each PAS-Na group was different from that of control group. However, there was no dose-response relationship between the two groups. Compared with the control group, the survival rate of neurons in manganese exposed group was significantly lower, and the percentage of DNA in comet tail increased. The survival rate of neurons in L-Mn group was increased, the percentage of comet tail DNA was decreased, the content of MDA was decreased, and the activity of SOD was increased. The difference was statistically significant (P 0.05, P 0.05, P < 0.05), and the survival rate of neurons in M-Mn group was increased after treatment with M-PAS (P 0.05, P 0.05, P < 0.05, P < 0.05, P 0.05, P < 0.05, P < 0.05, P < 0.05, P < 0.05, P < 0.05, P < 0.05, P < 0.05). The percentage of DNA in comet tail decreased with the decrease of Olive tail distance, and the difference was statistically significant (P 0.05). Conclusion Manganese exposure in vitro can significantly interfere with the damage of primary basal nucleus neurons in rats. PAS-Na has a certain effect on the toxicity of basal nucleus neurons induced by manganese.
【学位授予单位】：广西医科大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R114

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