Autor: |
Jason J. McDougall, Milind M. Muley, Holly T. Philpott, Allison Reid, Eugene Krustev |
Jazyk: |
angličtina |
Rok vydání: |
2017 |
Předmět: |
|
Zdroj: |
Arthritis Research & Therapy, Vol 19, Iss 1, Pp 1-9 (2017) |
Druh dokumentu: |
article |
ISSN: |
1478-6362 |
DOI: |
10.1186/s13075-017-1313-1 |
Popis: |
Abstract Background The endocannabinoid system has been shown to reduce inflammatory flares and pain in rodent models of arthritis. A limitation of endocannabinoids is that they are rapidly denatured by hydrolysing enzymes such as fatty acid amide hydrolase (FAAH) which renders them physiologically inert. Osteoarthritis (OA) is primarily a degenerative joint disease; however, it can incorporate mild inflammation and peripheral neuropathy. The aim of this study was to determine whether early blockade of FAAH bioactivity could reduce OA-associated inflammation and joint neuropathy. The ability of this treatment to prevent end-stage OA pain development was also tested. Methods Physiological saline or sodium monoiodoacetate (MIA; 0.3 mg) was injected into the right knee of male C57Bl/6 mice (20–42 g) and joint inflammation (oedema, blood flow and leukocyte trafficking) was measured over 14 days. Joint inflammation was also measured in a separate cohort of animals treated on day 1 with either saline or the FAAH inhibitor URB597 (0.03–0.3 mg/kg topical onto the knee joint). In other experiments, von Frey hair tactile sensitivity was determined on days 1 and 14 in MIA-injected mice treated prophylactically with URB597 (0.3 mg/kg s.c. over the knee joint on days 0–3). Saphenous nerve myelination was also assessed in these animals on day 14 by G-ratio analysis. Results Intra-articular injection of MIA caused an increase in joint oedema (P |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
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