{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,3]],"date-time":"2026-06-03T20:57:29Z","timestamp":1780520249775,"version":"3.54.1"},"reference-count":52,"publisher":"Wiley","issue":"2b","license":[{"start":{"date-parts":[[2011,8,28]],"date-time":"2011-08-28T00:00:00Z","timestamp":1314489600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2011,9,2]]},"abstract":"<jats:p><jats:bold>BACKGROUND AND PURPOSE<\/jats:bold> Huntington's disease (HD) is a progressive neurodegenerative disorder characterized by a degeneration of striatal neurons. The possible role of COX and lipoxygenase (LOX) pathways has been well\u2010documented in the pathology of several neurodegenerative disorders including HD. Licofelone is a competitive inhibitor of COX\u20101\u2013 and COX\u20102 and 5\u2010LOX isoenzymes. Therefore, the present study was designed to investigate possible neuroinflammatory and apoptotic mechanisms in the neuroprotective effect of licofelone against 3\u2010nitropropionic acid (3\u2010NP)\u2010induced HD\u2010like symptoms in rats.<\/jats:p><jats:p><jats:bold>EXPERIMENTAL APPROACH<\/jats:bold> Rats were administered 3\u2010NP (10\u2003mg\u00b7kg<jats:sup>\u22121<\/jats:sup>day<jats:sup>\u22121<\/jats:sup>, i.p.) for 14 days. Licofelone (2.5, 5 and 10\u2003mg\u00b7kg<jats:sup>\u22121<\/jats:sup>, p.o.) was given once a day, 1\u2003h before 3\u2010NP treatment for 14 days. Body weight and behavioural parameters (locomotor and rotarod activity) were assessed on the 1st, 5th, 10th and 15th day post\u20103\u2010NP administration. Malondialdehyde, nitrite concentration, endogenous antioxidant enzymes (superoxide dismutase and catalase levels), mitochondrial enzyme complexes, pro\u2010inflammatory compounds (TNF\u2010\u03b1, IL\u20106, NF\u2010\u03baB), PGs (PGE<jats:sub>2<\/jats:sub> and PGF<jats:sub>2\u03b1<\/jats:sub>) and caspase\u20103 activity were measured on day 15 in the striatum.<\/jats:p><jats:p><jats:bold>KEY RESULTS<\/jats:bold> Systemic 3\u2010NP treatment significantly reduced body weight, locomotor activity, oxidative defence, mitochondrial enzyme complex activities and increased TNF\u2010\u03b1, IL\u20106, caspase\u20103 activity, NF\u2010\u03baB and PGE<jats:sub>2<\/jats:sub> and PGF<jats:sub>2\u03b1<\/jats:sub> levels in the striatum. Licofelone (2.5, 5 and 10\u2003mg\u00b7kg<jats:sup>\u22121<\/jats:sup>) significantly attenuated the impairment in behavioural, biochemical and mitochondrial, pro\u2010inflammatory and pro\u2010apoptotic markers as compared with vehicle\u2010treated group.<\/jats:p><jats:p><jats:bold>CONCLUSIONS AND IMPLICATIONS<\/jats:bold> The results demonstrate the involvement of pro\u2010inflammatory compounds and the apoptotic cascade in the neuroprotective effect of licofelone against 3\u2010NP\u2010induced neurotoxicity.<\/jats:p>","DOI":"10.1111\/j.1476-5381.2011.01418.x","type":"journal-article","created":{"date-parts":[[2011,4,12]],"date-time":"2011-04-12T10:33:02Z","timestamp":1302604382000},"page":"644-654","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":101,"title":["Expression of Concern: Role of LOX\/COX pathways in 3\u2010nitropropionic acid\u2010induced Huntington's Disease\u2010like symptoms in rats: protective effect of 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