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目的探测N-乙酰半胱氨酸(NAC)对于组成型和诱导型表达mGlu1a所介导的兴奋性毒性的影响。方法在过表达mGlu1a的HEK293细胞中,通过免疫印迹法,MTT法,胎盘蓝排斥法,酶联免疫吸附实验,二氯荧光素检测法及HPLC等方法,探测了NAC对mGlu1a下游信号分子活性,细胞活力和凋亡,受体表面表达以及细胞内氧化应激的影响。结果发现受体的组成型和诱导型活性通过不同机制,参与了NAC对于mGlu1a所介导的兴奋性毒性的抑制。在以上两种情况下,NAC均可以通过降低ROS调节细胞内氧化还原电势。结论在不同生理刺激条件下,mGlu1a的活性对于疾病的发生可能起着不同的作用,尤其是对mGlu1a高表达所产生的效应,为探究与mGluI相关疾病的发生提供了理论依据。
Objective To investigate the effect of NAC on the excitotoxicity mediated by constitutive and inducible mGlu1a. Methods HEK293 cells overexpressing mGlu1a were used to detect the activity of NAC on downstream mGlu1a signaling molecules by Western blotting, MTT assay, placental blue exclusion assay, enzyme linked immunosorbent assay, dichlorofluorescein assay and HPLC. Cell viability and apoptosis, receptor surface expression and intracellular oxidative stress. As a result, the constitutive and inducible activities of the receptors were found to be involved in the inhibition of mGluIa-mediated excitotoxicity by NAC by different mechanisms. In both cases, NAC can regulate intracellular redox potential by decreasing ROS. Conclusion Under different physiological stimuli, the activity of mGlu1a may play different roles in the pathogenesis of the disease, especially the effect of mGlu1a overexpression, which provides a theoretical basis for exploring the occurrence of mGluI-related diseases.