Cipriani S, Bakshi R, Schwarzschild M A
Molecular Neurobiology Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, 114 16th street, Boston, MA 02129, USA.
Molecular Neurobiology Laboratory, MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, 114 16th street, Boston, MA 02129, USA.
Neuroscience. 2014 Aug 22;274:242-9. doi: 10.1016/j.neuroscience.2014.05.038. Epub 2014 May 29.
Inosine (hypoxanthine 9-beta-D-ribofuranoside), a purine nucleoside with multiple intracellular roles, also serves as an extracellular modulatory signal. On neurons, it can produce anti-inflammatory and trophic effects that confer protection against toxic influences in vivo and in vitro. The protective effects of inosine treatment might also be mediated by its metabolite urate. Urate in fact possesses potent antioxidant properties and has been reported to be protective in preclinical Parkinson's disease (PD) studies and to be an inverse risk factor for both the development and progression of PD. In this study we assessed whether inosine might protect rodent MES 23.5 dopaminergic cell line from oxidative stress in a cellular model of PD, and whether its effects could be attributed to urate. MES 23.5 cells cultured alone or in presence of enriched murine astroglial cultures MES 23.5-astrocytes co-cultures were pretreated with inosine (0.1-100 μM) for 24 h before addition of the oxidative stress inducer H₂O₂ (200 μM). Twenty-four hours later, cell viability was quantified by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay or immunocytochemistry in pure and MES 23.5-astrocytes co-cultures, respectively. H₂O₂-toxic effect on dopaminergic cells was reduced when they were cultured with astrocytes, but not when they were cultured alone. Moreover, in MES 23.5-astrocytes co-cultures, indicators of free radical generation and oxidative damage, evaluated by nitrite (NO₂(-)) release and protein carbonyl content, respectively, were attenuated. Conditioned medium experiments indicated that the protective effect of inosine relies on the release of a protective factor from inosine-stimulated astrocytes. Purine levels were measured in the cellular extract and conditioned medium using high-performance liquid chromatography (HPLC) method. Urate concentration was not significantly increased by inosine treatment however there was a significant increase in levels of other purine metabolites, such as adenosine, hypoxanthine and xanthine. In particular, in MES 23.5-astrocytes co-cultures, inosine medium content was reduced by 99% and hypoxanthine increased by 127-fold. Taken together these data raise the possibility that inosine might have a protective effect in PD that is independent of any effects mediated through its metabolite urate.
肌苷(次黄嘌呤9-β-D-呋喃核糖苷)是一种在细胞内具有多种作用的嘌呤核苷,也可作为细胞外调节信号。在神经元上,它能产生抗炎和营养作用,在体内和体外均可抵御毒性影响。肌苷治疗的保护作用可能也由其代谢产物尿酸介导。事实上,尿酸具有强大的抗氧化特性,并且在临床前帕金森病(PD)研究中已被报道具有保护作用,是PD发生和进展的反向风险因素。在本研究中,我们评估了肌苷是否能在PD细胞模型中保护啮齿动物MES 23.5多巴胺能细胞系免受氧化应激,以及其作用是否可归因于尿酸。单独培养的MES 23.5细胞或在富含小鼠星形胶质细胞培养物(MES 23.5 - 星形胶质细胞共培养物)存在的情况下培养的MES 23.5细胞,在添加氧化应激诱导剂过氧化氢(H₂O₂,200 μM)之前,先用肌苷(0.1 - 100 μM)预处理24小时。24小时后,分别通过3 -(4,5 - 二甲基噻唑 - 2 - 基)- 2,5 - 二苯基四氮唑溴盐(MTT)法或免疫细胞化学法对纯培养物和MES 23.5 - 星形胶质细胞共培养物中的细胞活力进行定量。当多巴胺能细胞与星形胶质细胞共培养时,H₂O₂对其的毒性作用降低,但单独培养时则不然。此外,在MES 23.5 - 星形胶质细胞共培养物中,分别通过亚硝酸盐(NO₂⁻)释放和蛋白质羰基含量评估的自由基生成和氧化损伤指标均减弱。条件培养基实验表明,肌苷的保护作用依赖于肌苷刺激的星形胶质细胞释放一种保护因子。使用高效液相色谱(HPLC)法测量细胞提取物和条件培养基中的嘌呤水平。肌苷处理后尿酸浓度没有显著增加,然而其他嘌呤代谢产物如腺苷、次黄嘌呤和黄嘌呤的水平有显著增加。特别是,在MES 23.5 - 星形胶质细胞共培养物中,肌苷培养基含量降低了99%,次黄嘌呤增加了127倍。综上所述,这些数据增加了一种可能性,即肌苷在PD中可能具有保护作用且独立于通过其代谢产物尿酸介导的任何作用。