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Gastrodin relieved complete Freund's adjuvant-induced spontaneous pain by inhibiting inflammatory response
Affiliation:1. Department of Pharmacology, School of Pharmacy, The Fourth Military Medical University, Xi''an, Shaanxi Province 710032, P.R.China;2. Department of Natural Medicine, Institute of Materia Medica, School of Pharmacy, The Fourth Military Medical University, Xi''an, Shaanxi Province 710032, P.R.China;3. Student Brigade, The Fourth Military Medical University, Xi''an, Shaanxi Province 710032, P.R.China;4. Department of Diagnostic Radiology, Tangdu Hospital, The Fourth Military Medical University, Xi''an, Shaanxi Province 710032, P.R.China;1. Department of Neurosurgery, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, China;2. Department of Neurosurgery, The First Affiliated Hospital, Wenzhou Medical University, Wenzhou 325000, China;1. Department of Psychology, The University of Texas at Arlington, TX 76019, USA;2. Department of Oral and Maxillofacial Surgery, University of California, San Francisco, CA 94143-0440, USA;3. Department of Pain Management, Tiantan Hospital, Beijing 100050, China;1. Division of Physiology, Department of Basic Sciences, Faculty of Veterinary Medicine, Urmia University, Urmia 5756151818, Iran;2. Division of Anatomy, Department of Basic Sciences, Faculty of Veterinary Medicine, Urmia University, Urmia 5756151818, Iran
Abstract:The analgesic effects of gastrodin (GAS), an active component derived from the Chinese herb Tian ma (Gastrodia elata Blume), on chronic inflammatory pain of mice and the involved molecular mechanisms were investigated. GAS significantly attenuated mice chronic inflammatory pain induced by hindpaw injection of complete Freund's adjuvant (CFA) and the accompanying anxiety-like behaviors. GAS administration reduced CFA-induced up-regulation of GluR1-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, GluN2A- and GluN2B-containing N-methyl-d-aspartate (NMDA) receptors, and Ca2 +/calmodulin-dependent protein kinase II-alpha (CaMKII-α) in the anterior cingulate cortex (ACC). The GluN2A and GluN2B subunits of NMDA receptors, the GluR1 type of AMPA receptor, and CaMKII-α are key molecules responsible for neuroplasticity involved in chronic pain and the accompanying anxiety. Moreover, GAS administration reduced the activation of astrocyte and microglia and the induction of TNF-α and IL-6 in the ACC of the CFA-injected mice. Therefore, GAS administration relieved chronic pain, exerted anxiolytic effects by regulating neuroplasticity molecules, and attenuated the inflammatory response by reducing the induction of TNF-α and IL-6 in the ACC of the CFA-injected mice.
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