Evidence for the Participation of Acid-Sensing Ion Channels (ASICs) in the Antinociceptive Effect of Curcumin in a Formalin-Induced Orofacial Inflammatory Model
Autor: | Huiling Yang, Dongyun Qin, Hui Fu, Yongfu Wu |
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Rok vydání: | 2016 |
Předmět: |
Nociception
0301 basic medicine Curcumin Antioxidant medicine.medical_treatment Action Potentials Inflammation Pharmacology Rats Sprague-Dawley 03 medical and health sciences Cellular and Molecular Neuroscience Trigeminal ganglion chemistry.chemical_compound 0302 clinical medicine Formaldehyde Ganglia Spinal medicine Extracellular Animals Acid-sensing ion channel Neurons Chemistry Cell Biology General Medicine Acid Sensing Ion Channels Disease Models Animal 030104 developmental biology Trigeminal Ganglion Face Hyperalgesia medicine.symptom 030217 neurology & neurosurgery |
Zdroj: | Cellular and Molecular Neurobiology. 37:635-642 |
ISSN: | 1573-6830 0272-4340 |
DOI: | 10.1007/s10571-016-0399-3 |
Popis: | Curcumin, a major bioactive component of turmeric, has diverse therapeutic effects such as anti-inflammatory, antioxidant, anticancer, and antinociceptive activities. The acid-sensing ion channels (ASICs), which can be activated by acute drops in the extracellular pH, play an important role in nociception. However, very little is known about the interaction between ASICs and curcumin in nociception of inflammation. In our study, we investigated whether the antinociceptive effects of curcumin are mediated via ASICs using an orofacial nociceptive model and in vitro western blotting, immunofluorescence, whole-cell patch-clamp recordings in the trigeminal system. Intraperitoneally administered curcumin at a dose of 50 mg/kg can reduce hyperalgesia in both the phases of a formalin-induced orofacial nociceptive model. Curcumin reduced the amplitude of ASICs currents in a dose-dependent manner in trigeminal ganglion (TG) neurons, and curcumin also reduced the protein quantity but did not change the distribution of ASICs in TG. Thus, our results indicate that curcumin can reduce formalin-induced ASICs activation and thus inhibit ASICs-mediated inflammatory pain hypersensitivity. |
Databáze: | OpenAIRE |
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