{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,5,13]],"date-time":"2025-05-13T21:50:18Z","timestamp":1747173018309,"version":"3.40.5"},"reference-count":46,"publisher":"Cambridge University Press (CUP)","issue":"5","license":[{"start":{"date-parts":[[2022,2,3]],"date-time":"2022-02-03T00:00:00Z","timestamp":1643846400000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/www.cambridge.org\/core\/terms"}],"content-domain":{"domain":["cambridge.org"],"crossmark-restriction":true},"short-container-title":["Acta Neuropsychiatr."],"published-print":{"date-parts":[[2022,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec id=\"S0924270822000035_as1\"><jats:title>Objective:<\/jats:title><jats:p>This study was aimed at evaluating the efficacy of glucosamine and potential mechanisms of actions in a neuropathic pain model in rats.<\/jats:p><\/jats:sec><jats:sec id=\"S0924270822000035_as2\"><jats:title>Methods:<\/jats:title><jats:p>Glucosamine (500, 1000 and 2000 mg\/kg) was administered via gavage route, 1 day before the chronic constriction injury (CCI) of sciatic nerve and daily for 14 days (prophylactic regimen), or from days 5 to 14 post-injury (therapeutic regimen), as the indicators of neuropathic pain, mechanical allodynia, cold allodynia and thermal hyperalgesia were assessed on days 0, 3, 5, 7, 10 and 14 after ligation. Inducible nitric oxide synthase (iNOS) and tumour necrosis factor alpha (TNF-\u03b1) gene expressions were measured by real-time polymerase chain reaction. TNF-\u03b1 protein content was measured using the enzyme-linked immunosorbent assay method.<\/jats:p><\/jats:sec><jats:sec id=\"S0924270822000035_as3\"><jats:title>Results:<\/jats:title><jats:p>Three days after nerve injury, the threshold of pain was declined among animals subjected to neuropathic pain. Mechanical and cold allodynia, as well as thermal hyperalgesia were attenuated by glucosamine (500, 1000, 2000 mg\/kg) in the prophylactic regimen. However, existing pain was not decreased by this drug. Increased mRNA expression of iNOS and TNF-\u03b1 was significantly reduced in the spinal cord of CCI animals by glucosamine (500, 1000, 2000 mg\/kg) in the prophylactic regimen. The overall expression of spinal TNF-\u03b1 was increased by CCI, but this increase was reduced in animals receiving glucosamine prophylactic treatment.<\/jats:p><\/jats:sec><jats:sec id=\"S0924270822000035_as4\"><jats:title>Conclusion:<\/jats:title><jats:p>Findings suggest that glucosamine as a safe supplement may be a useful candidate in preventing neuropathic pain following nerve injury. Antioxidant and anti-inflammatory effects may be at least in part responsible for the antinociceptive effects of this drug.<\/jats:p><\/jats:sec>","DOI":"10.1017\/neu.2022.3","type":"journal-article","created":{"date-parts":[[2022,2,3]],"date-time":"2022-02-03T02:53:21Z","timestamp":1643856801000},"page":"260-268","update-policy":"https:\/\/doi.org\/10.1017\/policypage","source":"Crossref","is-referenced-by-count":0,"title":["Antinociceptive effect of N-acetyl glucosamine in a rat model of neuropathic pain"],"prefix":"10.1017","volume":"34","author":[{"given":"Ehsan","family":"Mohebbi","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mehdi","family":"Molavi","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mohamadreza","family":"Amin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9121-7453","authenticated-orcid":false,"given":"Bahareh","family":"Amin","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Mohammad","family":"Sahebkar","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"56","published-online":{"date-parts":[[2022,2,3]]},"reference":[{"doi-asserted-by":"publisher","key":"S0924270822000035_ref44","DOI":"10.1016\/j.ejpain.2008.09.010"},{"doi-asserted-by":"publisher","key":"S0924270822000035_ref46","DOI":"10.4049\/jimmunol.175.11.7202"},{"key":"S0924270822000035_ref34","first-page":"33","article-title":"The liver-protective properties of D-glucosamine","volume":"53","author":"Sal'nikova","year":"1990","journal-title":"Farmakologiia i Toksikologiia"},{"doi-asserted-by":"publisher","key":"S0924270822000035_ref11","DOI":"10.4103\/0976-500X.119726"},{"doi-asserted-by":"publisher","key":"S0924270822000035_ref15","DOI":"10.4065\/mcp.2009.0649"},{"doi-asserted-by":"publisher","key":"S0924270822000035_ref22","DOI":"10.1016\/S1063-4584(03)00028-1"},{"doi-asserted-by":"publisher","key":"S0924270822000035_ref21","DOI":"10.1016\/j.pathophys.2013.04.003"},{"doi-asserted-by":"publisher","key":"S0924270822000035_ref25","DOI":"10.1016\/j.ejpain.2005.08.006"},{"key":"S0924270822000035_ref8","first-page":"2017","article-title":"Neuropeptides and microglial activation in inflammation, pain, and neurodegenerative diseases","volume":"5048616","author":"Carniglia","year":"2017","journal-title":"Mediators of Inflammation"},{"doi-asserted-by":"publisher","key":"S0924270822000035_ref27","DOI":"10.1111\/j.1749-6632.2000.tb06673.x"},{"doi-asserted-by":"publisher","key":"S0924270822000035_ref40","DOI":"10.1111\/j.1471-4159.2008.05614.x"},{"doi-asserted-by":"publisher","key":"S0924270822000035_ref41","DOI":"10.2147\/JPR.S138099"},{"doi-asserted-by":"publisher","key":"S0924270822000035_ref24","DOI":"10.1007\/s10787-017-0325-4"},{"doi-asserted-by":"publisher","key":"S0924270822000035_ref7","DOI":"10.1016\/0003-2697(76)90527-3"},{"doi-asserted-by":"publisher","key":"S0924270822000035_ref45","DOI":"10.1016\/j.intimp.2006.06.003"},{"key":"S0924270822000035_ref16","first-page":"385","article-title":"Synthetic analgesics. 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