摘要
目的探讨尿酸对6-羟基多巴(6-OHDA)介导的PC12细胞氧化损伤的作用。方法采用高分化PC12细胞制作帕金森病细胞模型,实验分为对照组、6-OHDA组、尿酸(Uricacid,UA)组和6-OHDA+UA组。药物作用6h、12h和24h,采用比色法检测细胞超氧化物歧化酶(SOD)的活性和乳酸脱氢酶(LDH)活力,硫代巴比妥酸法测定细胞内脂质过氧化产物丙二醛(MDA)的含量。结果 100μmol/L6-OHDA作用于PC12细胞12h、24h后,与对照组相比,SOD活性降低,LDH释放增加,MDA生成增多(P<0.05);UA组与对照组相比各项指标均无统计学差异(P>0.05);6-OHDA+UA组与6-OHDA组相比,SOD活性升高,LDH释放显著降低、MDA的生成减少(P<0.05)。结论尿酸具有减轻6-OHDA介导的PC12细胞损伤,其作用机制可能与提高SOD活性有关。
Objective To investigate the protective role of uric acid （UA） in oxidative injury induced by 6-hydroxydopamine （6-OHDA） in PC12 cells. Methods The highly differentiated PC12 cells were divided into 4 groups： the control, 6-OHDA, UA and 6-OHDA ＋UA. Each group was subdivided into 3 subgroups and cultured for 6, 12 and 24 hours in vitro, respectively. The content of Lactate dehydrogenas （LDH）, SOD in the culture medium, and intracellular malondialdehyde （MDA） were detected. Results The release of LDH and content of MDA in the group treated with 100 Ix mol/L 6-OHDA for 12 and 24 h were significantly increased compared with the control group, while the activity of SOD was decreased, which were reversed by 200 Ix mol/L UA treatment. Conclusion These results suggest that UA treatment can prevent PCI2 cell from oxidative stress-mediated injury, which may associated with the increased activity of SOD.
出处
《分子诊断与治疗杂志》
2011年第2期96-99,共4页
Journal of Molecular Diagnostics and Therapy
基金
江苏省自然科学基金(BK2010229)
江苏省高校自然研究计划项目(08KJB320012)
苏州市科技发展计划(社会发展及医药)项目(200815404)
