Pre-incubation of fibroblast-like cells with the cannabinoid receptor 1 (CB) antagonist SR141716A (1 μM) for 10 minutes prior to exposure to HU210 (for a further 10 minutes, 0

1 μM) significantly blocked HU210-induced phosphorylation of p44 (ERK1) and p42 (ERK2). The cannabinoid receptor 2 (CB) antagonist SR144528 (1 μM) did not significantly alter HU210-induced phosphorylation of p44 (ERK1) and p42 (ERK2). Data are expressed as immunoblots with levels of phosphorylated mitogen-activated protein kinase (MAPK) in the top band and total loading of protein below and as mean percentage of the unstimulated basal levels of MAPK phosphorylation ± standard error of the mean (n = 3 synovia). Comparison between drug treatment groups was carried out using one-way analysis of variance. **< 0.05 versus HU210. ERK, extracellular signal-regulated kinase.Copyright information:Taken from "Characterisation of the cannabinoid receptor system in synovial tissue and fluid in patients with osteoarthritis and rheumatoid arthritis"http://arthritis-research.com/content/10/2/R43Arthritis Research & Therapy 2008;10(2):R43-R43.Published online 16 Apr 2008PMCID:PMC2453762.