6-羥基多巴胺論文：尿酸減輕6-OHDA介導(dǎo)PC12細(xì)胞氧化損傷作用機(jī)制的研究

1、6-羥基多巴胺論文：尿酸減輕6-0HDA介導(dǎo)PC12細(xì)胞氧化損 傷作用機(jī)制的研究【中文摘要】 第一部分尿酸減輕6-0HDA寸PC12細(xì)胞的氧化損傷 作用：評(píng)價(jià)尿酸減輕6-0HDA寸PC12細(xì)胞的氧化損傷作用。 方法：采用 高分化PC12細(xì)胞制作帕金森病細(xì)胞模型，分為對(duì)照組(PBS組)、6-OHDA(10Qx mol.L-1)組、尿酸(200卩mol.L-1)組和6-OHDA(10mol.L-1)+尿酸(200卩mol.L-1)組,分別作用于6h、12h和24h。采用 比色法檢測(cè)乳酸脫氫酶(LDH釋放量,ELISA法測(cè)定8-羥基脫氧鳥(niǎo)苷(8-hydroxy 2-deoxyguanosine,8-

2、OHdG)含量,硫代巴比妥酸法測(cè) 定脂質(zhì)過(guò)氧化物丙二醛(MDA含量。結(jié)果:100卩molL-1 6-OHDA作 用于PC12細(xì)胞12h、24h后，與對(duì)照組相比,LDH釋放顯著增加(757.57士27.77 U/L vs175.57士10.50 U/L,874.83士16.93 U/L vs 161.76士9.71 U/L,P0.05)、8-OHdG生成增多(66.554.08 ng/L vs 19.61士2.04 ng/L,82.88士5.40ng/L vs 20.97ng/L5.14 ng/L,P0.05)、MDAfe成量顯著增加(2.96士0.14卩mol/g pro vs 0.67士0.

3、10卩mol/gpro,4.22士0.35卩mol/g pro vs 0.68士0.09卩mol/g pro,P0.05);6-OHDA+尿酸組與6-OHDA組相比丄DH釋放顯著降低(472.73士18.18 U/L vs 757.57士27.77 U/L,522.25士16.37U/L vs 874.83士16.93U/L,P0.05)、8-OHdG含量下降(51.59士3.12ng/L vs 66.55士4.08 ng/L,63.83士4.25 ng/L vs82.88士5.40 ng/L,P0.05)、MDA生成減少(2.08士0.29卩mol/g pro vs2.96士0.14卩mol

4、/g pro,2.55士0.36卩mol/g pro vs 4.22士0.35卩mol/g pro,P0.05)。結(jié)論：尿 酸對(duì)6-OHDA介導(dǎo)的PC12細(xì)胞氧化損傷具有保護(hù)作用。第二部分尿酸 減輕6-OHDA介導(dǎo)的PC12細(xì)胞SOD及GSH舌性下降：探討尿酸減輕6-OHDA介導(dǎo)的PC12細(xì)胞氧化損傷機(jī)制。方法：采用高分化PC12細(xì)胞 制作帕金森病細(xì)胞模型，分為對(duì)照組(PBS組)、6-OHDA(10(Vmol.L-1)組、尿酸(200卩mol.L-1)組和6-OHDA(10mol丄-1)+尿酸(200卩molL-1)組。6-OHDA分別作用于6h、12h、24h,比色法測(cè)定超氧化物 歧化酶(S

5、OD和【英文摘要】PARTI Protective effects of uric acid against6-OHDA-induced cell injury in PC12 cells through antioxidantacti on To inv estigate the protective effects of uric acid onthe injury of oxidative stress in duced by 6-hydroxydopam ine(6-OHDA in PC12cells.Methods The highly differentiatedPC12cells

6、 were divided into 4 groups: the control(the PBSgroup),6-hydroxydopamine(6-OHDA , uric acid(UA and 6-OHDA+UA. Eachgroup was subdivided into a further 3 subgroups and cultured for 6, 12 and24 hours in vitro respectively. The content of Lactate dehydrogenas(LDH , 8-hydroxy 2-deoxyguanosine(8-OHdG in t

7、he culture medium andintracellular malondialdehyde(MDA were detected.ResultsThe release of LDHin the group treated with 100 mol丄-1 6-OHDAfor 12h and 24 h were sig ni fica ntlyin creased compared with thecontrol group(757.57士27.77 U/L vs 175.57士10.50 U/L, 874.83士16.93 U/L vs 161.76士9.71 U/L, P0.05),

8、the contents of8-OHdGwas sig ni fica ntlyin creased(66.55士4.08 n g/L vs 19.61士2.04 ng/L, 82.88士5.40 ng/L vs 20.97士5.14 ng/L, P0.05),the levelof MDAwas also in creased(2.96士0.13卩mol/g pro vs 0.67士0.10mol/g pro,4.22士0.35卩mol/g pro vs 0.68士0.09卩mol/g pro,P0.05). However, there was no differenee on the

9、levels of LDH, 8-OHdGand MDA between UA group and the con trol group.While the release ofLDH was decreased(472.73士18.18U/L vs 757.57士27.77 U/L, 522.25士16.37 U/L vs 874.83士16.93 U/L,P0.05), contents of 8-OHdGwas decreased(51.59士3.12 ng/L vs 66.55士4.08 ng/L,63.83士4.25 ng/L vs 82.88士5.40 ng/L, P0.05),

10、contentsof MDA was also decreased(2.08士0.29卩mol/g pro vs 2.96士0.14卩mol/g pro, 2.55士0.36卩mol/g pro vs 4.22士0.35mol/g pro, P0.05)in 6-OHDA+UA group comparedwith 6-OHDA group.Conclusion Uric acid can prevent PC12 cells fromoxidative stress in duced by 6-hydroxydopam ine(6-OHDA .PARTEThe protective role of uric acid in the6-OHDA-mediated PC