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Details

Autor(en) / Beteiligte
Titel
Gastrodin relieved complete Freund's adjuvant-induced spontaneous pain by inhibiting inflammatory response
Ist Teil von
  • International immunopharmacology, 2016-12, Vol.41, p.66-73
Ort / Verlag
Netherlands: Elsevier B.V
Erscheinungsjahr
2016
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
  • 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. •Gastrodin (GAS) relieved chronic inflammatory pain and anxiety-like behaviors induced by Complete Freund’s adjuvant (CFA).•GAS inhibited the enhanced expression of GluR1, GluN2A, GluN2B and CaMKII-α in anterior cingulate cortex (ACC) of CFA-mice.•GAS administration inhibited the activation of astrocytes and microglia in the ACC of CFA-injected mice.•GAS treatment reduced the induction of TNF-α and IL-6 in the ACC of CFA-injected mice.
Sprache
Englisch
Identifikatoren
ISSN: 1567-5769
eISSN: 1878-1705
DOI: 10.1016/j.intimp.2016.10.020
Titel-ID: cdi_proquest_miscellaneous_1837029522
Format
Schlagworte
ACC, Amino acids, Analgesics, Analgesics - pharmacology, Analgesics - therapeutic use, Animals, Anti-Anxiety Agents - pharmacology, Anti-Anxiety Agents - therapeutic use, Anti-Inflammatory Agents - pharmacology, Anti-Inflammatory Agents - therapeutic use, Anxiety, Anxiety - drug therapy, Anxiety - metabolism, Astrocytes - drug effects, Astrocytes - metabolism, Benzyl Alcohols - pharmacology, Benzyl Alcohols - therapeutic use, Ca2+/calmodulin-dependent protein kinase II, Calcium, Calcium-binding protein, Calcium-Binding Proteins - metabolism, Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism, Calmodulin, CFA, Chemical compounds, Chronic inflammatory pain, Cortex (cingulate), Freund's Adjuvant, Gastrodin, Glial Fibrillary Acidic Protein - metabolism, Glucosides - pharmacology, Glucosides - therapeutic use, Glutamic acid receptors (ionotropic), Gyrus Cinguli - drug effects, Gyrus Cinguli - metabolism, Herbs, Hot Temperature, Hyperalgesia - chemically induced, Hyperalgesia - drug therapy, Hyperalgesia - metabolism, IL-6, Inflammation, Inflammatory response, Interleukin 6, Interleukin-6 - metabolism, Male, Mice, Mice, Inbred C57BL, Microfilament Proteins - metabolism, Microglia, Microglia - drug effects, Microglia - metabolism, Molecular modelling, Molecules, N-Methyl-D-aspartic acid receptors, Neuroplasticity, Pain, Pain - chemically induced, Pain - drug therapy, Pain - metabolism, Plasticity, Receptors, Receptors, AMPA - metabolism, Receptors, N-Methyl-D-Aspartate - metabolism, Rodents, TNF-α, Touch, Tumor necrosis factor, Tumor Necrosis Factor-alpha - metabolism, Tumor necrosis factor-TNF, α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid, α-Amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors

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