Radad Khaled, Moldzio Rudolf, Taha Mokhtar, Rausch Wolf-Dieter
Pathology Department, Faculty of Veterinary Medicine, Assiut University, Assiut, Egypt.
Phytother Res. 2009 May;23(5):696-700. doi: 10.1002/ptr.2708.
Thymoquinone is the main active constituent of Nigella sativa seeds with antioxidant and antiinflammatory properties. In the present study, primary dopaminergic cultures from mouse mesencephala were used to investigate the neuroprotective effects of thymoquinone against MPP(+) and rotenone toxicities. MPP(+) (10 microm on day 10 in vitro (i.v.) for 48 h) significantly decreased the number of THir by 40% compared with untreated control cultures. Rotenone at both short (20 nm on day 10 i.v. for 48 h) and long-term (1 nm on day 6 i.v. for 6 consecutive days) toxicities reduced the number of THir neurons by 33% and 24%, respectively. Treatment of cultures with thymoquinone (0.01, 0.1, 1, 10 microm on day 8 i.v. for 4 days) rescued about 25% of THir neurons at concentrations of 0.1 microm and 1 microm against MPP(+)-induced cell death. Against rotenone, thymoquinone afforded significant protection in both short- and long-term models. In short-term rotenone toxicity, thymoquinone (from days 8-12 i.v.) saved about 65%, 74% and 79% of THir neurons at concentrations of 0.01, 0.1 and 1 microm, respectively, compared with cell loss induced by rotenone. In long-term rotenone toxicity, concomitant treatment of cultures with thymoquinone significantly rescued about 83-100% of THir neurons compared with rotenone-treated cultures. In conclusion, the current study presents for the first time the potential of thymoquinone to protect primary dopaminergic neurons against MPP(+) and rotenone relevant to Parkinson's disease.
百里醌是黑种草籽的主要活性成分，具有抗氧化和抗炎特性。在本研究中，使用来自小鼠中脑的原代多巴胺能培养物来研究百里醌对MPP(+)和鱼藤酮毒性的神经保护作用。与未处理的对照培养物相比，MPP(+)(体外培养第10天静脉注射10微摩尔，持续48小时)使THir数量显著减少40%。短期(体外培养第10天静脉注射20纳米，持续48小时)和长期(体外培养第6天静脉注射1纳米，连续6天)鱼藤酮毒性分别使THir神经元数量减少33%和24%。用百里醌(体外培养第8天静脉注射0.01、0.1、1、10微摩尔，持续4天)处理培养物，在0.1微摩尔和1微摩尔浓度下可挽救约25%的THir神经元免受MPP(+)诱导的细胞死亡。对于鱼藤酮，百里醌在短期和长期模型中均提供了显著保护。在短期鱼藤酮毒性模型中，与鱼藤酮诱导的细胞损失相比，百里醌(体外培养第8 - 12天静脉注射)在0.01、0.1和1微摩尔浓度下分别挽救了约65%、74%和79%的THir神经元。在长期鱼藤酮毒性模型中，与鱼藤酮处理的培养物相比，用百里醌同时处理培养物可显著挽救约83 - 100%的THir神经元。总之，本研究首次展示了百里醌保护原代多巴胺能神经元免受与帕金森病相关的MPP(+)和鱼藤酮毒性影响的潜力。
