本文選題：錳 + 對氨基水楊酸鈉　； 參考：《廣西醫(yī)科大學(xué)》2013年碩士論文

【摘要】：目的探討對氨基水楊酸鈉(PAS-Na)對體外錳致大鼠原代基底核神經(jīng)元損傷的影響。材料與方法培養(yǎng)至第8天的基底核神經(jīng)元隨機分為正常對照組(對照組)、低、中、高劑量染錳(L-、M-、H-Mn)組、PAS-Na (PAS)對照組、低、中、高劑量PAS-Na (L-、M-、H-PAS)干預(yù)組。對照組神經(jīng)元給予培養(yǎng)液培養(yǎng)24h；染錳組神經(jīng)元暴露于MnCl2·4H2O100、200、400μ mol/L培養(yǎng)液培養(yǎng)24h; PAS對照組神經(jīng)元給予含PAS-Na50、500、5000μ mol/L培養(yǎng)液培養(yǎng)24h。L-、M-、H-PAS干預(yù)組神經(jīng)元分別暴露于MnCl2·4H2O100、200、400μ mol/L培養(yǎng)液培養(yǎng)24h,接著棄掉原培養(yǎng)液,再分別給予含PAS-Na50、500、5000μ mol/L的培養(yǎng)液培養(yǎng)24h。其余組培養(yǎng)液培養(yǎng)24h。然后,用噻唑藍(MTT)法測定存活率,單細胞凝膠電泳技術(shù)(SCGE)測定DNA損傷,硫代巴比妥酸(TBA)測定丙二醛(MDA),水溶性四唑鹽(WST-1)法測定測定超氧化物歧化酶(SOD)活力。結(jié)果(1)錳可引起基底核神經(jīng)元形態(tài)損傷和存活率呈劑量-反應(yīng)性下降。(2)PAS-Na對基底核神經(jīng)元形態(tài)無明顯影響,各PAS-Na劑量組的存活率與對照組有差異,但組間無劑量-反應(yīng)關(guān)系。(3)與對照組相比,染錳組神經(jīng)元存活率明顯降低,彗星尾部DNA百分率、Olive尾距增高,MDA含量增加,SOD活力下降,差異有統(tǒng)計學(xué)意義(P0.05)。(4) L-、M-PAS干預(yù)使暴露于L-Mn組神經(jīng)元存活率提高,彗星尾部DNA百分率、Olive尾距降低,MDA含量減少,SOD活力增高,差異有統(tǒng)計學(xué)意義(P0.05)。(5)M-PAS干預(yù)使暴露于M-Mn組神經(jīng)元存活率提高,彗星尾部DNA百分率、Olive尾距降低,SOD活力增高,差異有統(tǒng)計學(xué)意義(P0.05)。結(jié)論體外染錳對大鼠原代基底核神經(jīng)元損傷明顯,PAS-Na對錳致基底核神經(jīng)元毒性有一定的干預(yù)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.
【學(xué)位授予單位】：廣西醫(yī)科大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2013
【分類號】：R114

【參考文獻】

相關(guān)期刊論文 前10條

1 王芳;王禪;姜岳明;鄧祥發(fā);陸繼培;區(qū)仕燕;;對氨基水楊酸鈉干預(yù)錳致大鼠海馬神經(jīng)元損傷的體外研究[J];工業(yè)衛(wèi)生與職業(yè)病;2011年02期

2 劉，

本文編號：1848433