rn-1734 has been researched along with Pain* in 4 studies
1 review(s) available for rn-1734 and Pain
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TRPV4: new therapeutic target for inflammatory bowel diseases.
The transient receptor potential vanilloid-4 (TRPV4) belongs to a family of ion channels and can be activated by warm temperature, hypotonicity, cell swelling or lipid mediators of the arachidonic cascade. The metabolites or events responsible for TRPV4 activation are associated with inflammation, arguing in favor of a role for this receptor in inflammatory diseases. The first studies have focused their attention on the role of TRPV4 in neurons and endothelial cells but TRPV4 cellular distribution is widespread, particularly in the gastrointestinal tract. Herein, we review a number of studies demonstrating the expression of TRPV4 in the gut, the regulation of its expression and functions by inflammatory mediators in that organ and the consequences of TRPV4 activation or inhibition in the intestine. We further discuss the relevance of considering this receptor as a potential target for therapeutic development in inflammatory bowel diseases. Topics: Animals; Drug Delivery Systems; Humans; Inflammation Mediators; Inflammatory Bowel Diseases; Intestinal Mucosa; Pain; Sulfonamides; TRPV Cation Channels | 2014 |
3 other study(ies) available for rn-1734 and Pain
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Endothelin-1 Elicits TRP-Mediated Pain in an Acid-Induced Oral Ulcer Model.
Oral ulcer is the most common oral disease and leads to pain during meals and speaking, reducing the quality of life of patients. Recent evidence using animal models suggests that oral ulcers induce cyclooxygenase-dependent spontaneous pain and cyclooxygenase-independent mechanical allodynia. Endothelin-1 is upregulated in oral mucosal inflammation, although it has not been shown to induce pain in oral ulcers. In the present study, we investigated the involvement of endothelin-1 signaling with oral ulcer-induced pain using our proprietary assay system in conscious rats. Endothelin-1 was significantly upregulated in oral ulcers experimentally induced by topical acetic acid treatment, while endothelin-1 production was suppressed by antibacterial pretreatment. Spontaneous nociceptive behavior in oral ulcer model rats was inhibited by swab applications of BQ-788 (ET Topics: Acetanilides; Anilides; Animals; Bridged Bicyclo Compounds; Caproates; Cinnamates; Disease Models, Animal; Endothelin-1; Male; Oligopeptides; Oral Ulcer; Pain; Peptides, Cyclic; Piperidines; Purines; Rats; Rats, Wistar; Signal Transduction; Sulfonamides; TRPV Cation Channels | 2018 |
Prostanoid-dependent spontaneous pain and PAR
During dental treatments, intraoral appliances frequently induce traumatic ulcers in the oral mucosa. Such mucosal injury-induced mucositis leads to severe pain, resulting in poor quality of life and decreased cooperation in the therapy. To elucidate mucosal pain mechanisms, we developed a new rat model of intraoral wire-induced mucositis and investigated pain mechanisms using our proprietary assay system for conscious rats. A thick metal wire was installed in the rats between the inferior incisors for one day. In the mucosa of the mandibular labial fornix region, which was touched with a free end of the wire, traumatic ulcer and submucosal abscess were induced on day 1. The ulcer was quickly cured until next day and abscess formation was gradually disappeared until five days. Spontaneous nociceptive behavior was induced on day 1 only, and mechanical allodynia persisted over day 3. Antibiotic pretreatment did not affect pain induction. Spontaneous nociceptive behavior was sensitive to indomethacin (cyclooxygenase inhibitor), ONO-8711 (prostanoid receptor EP1 antagonist), SB-366791, and HC-030031 (TRPV1 and TRPA1 antagonists, respectively). Prostaglandin E2 and 15-deoxyΔ12,14-prostaglandin J2 were upregulated only on day 1. In contrast, mechanical allodynia was sensitive to FSLLRY-NH2 (protease-activated receptor PAR2 antagonist) and RN-1734 (TRPV4 antagonist). Neutrophil elastase, which is known as a biased agonist for PAR2, was upregulated on days 1 to 2. These results suggest that prostanoids and PAR2 activation elicit TRPV1- and TRPA1-mediated spontaneous pain and TRPV4-mediated mechanical allodynia, respectively, independently of bacterial infection, following oral mucosal trauma. The pathophysiological pain mechanism suggests effective analgesic approaches for dental patients suffering from mucosal trauma-induced pain. Topics: Acetanilides; Animals; Bridged Bicyclo Compounds; Caproates; Hyperalgesia; Male; Pain; Prostaglandins; Purines; Rats, Wistar; Receptor, PAR-2; Sulfonamides; TRPA1 Cation Channel; TRPV Cation Channels | 2017 |
Transient receptor potential vanilloid 4 blockade protects against experimental colitis in mice: a new strategy for inflammatory bowel diseases treatment?
Recent reports suggested that the activation of Transient Receptor Potential Vanilloid 4 (TRPV4) receptors in the gastrointestinal tract has pro-inflammatory effects. In this study, we demonstrated for the first time that TRPV4 mRNA expression is up-regulated in patients with inflammatory bowel diseases (IBD). Furthermore, selective blockade of TRPV4 in the 2,4,6-trinitrobenzenesulfonic acid animal model alleviates colitis and pain associated with the intestinal inflammation. Our study indicates that TRPV4 may play a role in mechanisms of defense in intestinal inflammation and that TRPV4 may be an attractive target for future systemic or topic anti-inflammatory treatment in patients with IBD. Topics: Animals; Disease Models, Animal; Gastrointestinal Agents; Humans; Inflammatory Bowel Diseases; Mice; Pain; Real-Time Polymerase Chain Reaction; Reverse Transcriptase Polymerase Chain Reaction; Sulfonamides; TRPV Cation Channels | 2012 |