Ding Xue-Feng, Wu Yan, Qu Wen-Rui, Fan Ming, Zhao Yong-Qi
Department of Cognitive Sciences, Beijing Institute of Basic Medical Sciences, Beijing, China.
Hand & Foot Surgery and Reparative & Reconstructive Surgery Center, Orthopedic Hospital of the Second Hospital of Jilin University, Changchun, Jilin Province, China.
Neural Regen Res. 2018 Mar;13(3):449-455. doi: 10.4103/1673-5374.228727.
Quinacrine, widely used to treat parasitic diseases, binds to cell membranes. We previously found that quinacrine pretreatment reduced microwave radiation damage in rat hippocampal neurons, but the molecular mechanism remains poorly understood. Considering the thermal effects of microwave radiation and the protective effects of quinacrine on heat damage in cells, we hypothesized that quinacrine would prevent microwave radiation damage to cells in a mechanism associated with cell membrane stability. To test this, we used retinoic acid to induce PC12 cells to differentiate into neuron-like cells. We then pretreated the neurons with quinacrine (20 and 40 mM) and irradiated them with 50 mW/cm microwaves for 3 or 6 hours. Flow cytometry, atomic force microscopy and western blot assays revealed that irradiated cells pretreated with quinacrine showed markedly less apoptosis, necrosis, and membrane damage, and greater expression of heat shock protein 70, than cells exposed to microwave irradiation alone. These results suggest that quinacrine stabilizes the neuronal membrane structure by upregulating the expression of heat shock protein 70, thus reducing neuronal injury caused by microwave radiation.
广泛用于治疗寄生虫病的奎纳克林可与细胞膜结合。我们之前发现，奎纳克林预处理可减少大鼠海马神经元的微波辐射损伤，但其分子机制仍知之甚少。考虑到微波辐射的热效应以及奎纳克林对细胞热损伤的保护作用，我们推测奎纳克林可能通过与细胞膜稳定性相关的机制来预防微波辐射对细胞的损伤。为验证这一点，我们使用视黄酸诱导PC12细胞分化为神经元样细胞。然后用奎纳克林（20和40 mM）对神经元进行预处理，并用50 mW/cm的微波照射3或6小时。流式细胞术、原子力显微镜和蛋白质印迹分析显示，与仅接受微波照射的细胞相比，用奎纳克林预处理的照射细胞凋亡、坏死和膜损伤明显减少，热休克蛋白70的表达更高。这些结果表明，奎纳克林通过上调热休克蛋白70的表达来稳定神经元膜结构，从而减少微波辐射引起的神经元损伤。
