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Resolution: standard / high Figure 7.
Pre-incubation of fibroblast-like cells with the cannabinoid receptor 1 (CB1) 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 (CB2) antagonist SR144528 (1 μM) did not significantly alter HU210-induced phosphorylation
of p44 (ERK1) and p42 (ERK2). Data are expressed as (a) immunoblots with levels of phosphorylated mitogen-activated protein kinase (MAPK)
in the top band and total loading of protein below and as (b) 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. **P < 0.05 versus HU210. ERK, extracellular signal-regulated kinase.
Richardson et al. Arthritis Research & Therapy 2008 10:R43 doi:10.1186/ar2401 |