gingerol has been researched along with Pain* in 3 studies
3 other study(ies) available for gingerol and Pain
| Article | Year |
|---|---|
[6]-gingerol and [6]-shogaol, active ingredients of the traditional Japanese medicine hangeshashinto, relief oral ulcerative mucositis-induced pain via action on Na
Topics: Analgesics; Animals; Catechols; Cell Line; Drugs, Chinese Herbal; Fatty Alcohols; HEK293 Cells; Herbal Medicine; Humans; Male; Medicine, East Asian Traditional; Mucositis; Pain; Pain Management; Plant Extracts; Rats; Rats, Wistar; Sodium Channels | 2017 |
Analgesic and anti-inflammatory activities of [6]-gingerol.
In the present study, the analgesic and anti-inflammatory effects of [6]-gingerol, which is the pungent constituent of ginger, were performed. Intraperitoneal administration of [6]-gingerol (25 mg/kg-50 mg/kg) produced an inhibition of acetic acid-induced writhing response and formalin-induced licking time in the late phase. [6]-Gingerol (50 mg/kg-100 mg/kg) also produced an inhibition of paw edema induced by carrageenin. These results suggested that [6]-gingerol possessed analgesic and anti-inflammatory activities. Topics: Acetic Acid; Analgesics; Animals; Anti-Inflammatory Agents; Carrageenan; Catechols; Edema; Fatty Alcohols; Formaldehyde; Hindlimb; Male; Mice; Mice, Inbred ICR; Pain; Phytotherapy; Time Factors; Zingiber officinale | 2005 |
Noxious cold ion channel TRPA1 is activated by pungent compounds and bradykinin.
Six members of the mammalian transient receptor potential (TRP) ion channels respond to varied temperature thresholds. The natural compounds capsaicin and menthol activate noxious heat-sensitive TRPV1 and cold-sensitive TRPM8, respectively. The burning and cooling perception of capsaicin and menthol demonstrate that these ion channels mediate thermosensation. We show that, in addition to noxious cold, pungent natural compounds present in cinnamon oil, wintergreen oil, clove oil, mustard oil, and ginger all activate TRPA1 (ANKTM1). Bradykinin, an inflammatory peptide acting through its G protein-coupled receptor, also activates TRPA1. We further show that phospholipase C is an important signaling component for TRPA1 activation. Cinnamaldehyde, the most specific TRPA1 activator, excites a subset of sensory neurons highly enriched in cold-sensitive neurons and elicits nociceptive behavior in mice. Collectively, these data demonstrate that TRPA1 activation elicits a painful sensation and provide a potential molecular model for why noxious cold can paradoxically be perceived as burning pain. Topics: Acrolein; Animals; Behavior, Animal; Bradykinin; Cell Membrane; CHO Cells; Cold Temperature; Cricetinae; Dose-Response Relationship, Drug; Humans; Inflammation Mediators; Ion Channels; Membrane Potentials; Mice; Neurons, Afferent; Nociceptors; Pain; Pain Measurement; Rats; Transient Receptor Potential Channels; TRPA1 Cation Channel; Type C Phospholipases | 2004 |