Neuroprotective Effects of Etidronate and 2,3,3-Trisphosphonate Against Glutamate-Induced Toxicity in PC12 Cells

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• 作者：Wen Li ; Yuen-Ki Cheong ; Hui Wang ; Guogang Ren ; Zhuo Yang
• 关键词：Etidronate ; 2 ; 3 ; 3 ; Trisphosphonate ; PC12 cells ; Glutamate ; Neuroprotection
• 刊名：Neurochemical Research
• 出版年：2016
• 出版时间：April 2016
• 年：2016
• 卷：41
• 期：4
• 页码：844-854
• 全文大小：2,165 KB
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• 作者单位：Wen Li (1)
  Yuen-Ki Cheong (2)
  Hui Wang (3)
  Guogang Ren (2)
  Zhuo Yang (1)
  
  1. School of Medicine, State Key Laboratory of Medicinal Chemical Biology, Key Laboratory of Tumor Microenvironment and Neurovascular Regulation, Nankai University, 94 Weijin Road, Tianjin, 300071, China
  2. Science and Technology Research Institute, University of Hertfordshire, Hatfield, Herts, AL10 9AB, UK
  3. College of Life Sciences, Nankai University, 94 Weijin Road, Tianjin, 300071, China
  
• 刊物类别：Biomedical and Life Sciences
• 刊物主题：Biomedicine
  Neurosciences
  Biochemistry
  Neurology
  
• 出版者：Springer Netherlands
• ISSN：1573-6903

文摘

Etidronate is one of the best known bisphosphonates (BP) derivatives. It is often used as a reference drug in research related to hypercalcaemia and other common bone diseases. 2,3,3-trisphosphonate (TrisPP) is brand new analogue of BP, that also contains a ‘germinal bisphosphonate’ unit with an additional phosphoryl group attached in proximity to the BP unit. It is known that BPs bind to calcium by chemisorptions to form Ca-BP complexes through (O)P–C–P(O) moiety and hydrogen coordinations, and so they suppress calcium flow by interfering with Ca2+ channel operations. The mechanistic actions of BP, involving interactions and regulations of Ca2+, are somewhat similar to the pathogenesis of well-known neurodegenerative disorders, such as Alzheimer’s disease, Parkinson’s disease and Huntington’s disease. To investigate if neuroprotective effects are exhibited by the compounds of interests, we used a rat adrenal pheochromocytoma cell line (PC12) as our in vitro model to observe any occurrence of neuron inter-reflection. We pre-treated these PC12 cells with etidronate and TrisPP before challenging the cells with a high concentration of the neurotoxin, glutamate. Our data showed that pre-treatment with 100 μM etidronate partially ameliorated the glutamate-induced decrease in cell viability (47 %), whereas pre-treating cells with 10–100 μM TrisPP showed remarkable cell protection (78–86 %). Moreover, pre-treatments of the cells with etidronate or TrisPP attenuated cell apoptosis, reactive oxygen species generation, Ca2+ overloading and caspase-3 protein expression, which were associated with a remarkable increase in superoxide dismutase activity in our glutamate-injured PC12 cells. Therefore, this study supports the notion that etidronate and TrisPP may be promising neuroprotective agents.