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. 2016 Jan 27;7(6):6436–6447. doi: 10.18632/oncotarget.7042

Figure 4. Activation of CB2 receptors by THC stimulates IL-10 release and the ERK pathway in BM-MSCs.

Figure 4

THC treatment (1 μM, 24 h) induced significant elevation of the anti-inflammatory IL-10 release a., intracellular IL-10 protein expression b., c., and stimulated p-ERK1/2 expression d., e. The release of IL-10 from BM-MSCs was measured by ELISA. The protein expressions of intracellular IL-10 and p-ERK1/2 were analyzed by western blot analysis and normalized to GAPDH. Meanwhile, THC treatment significantly caused CB2 receptor expression in BM-MSCs f., g. CB2 antagonist, AM 630, greatly blocked the THC-induced elevation of IL-10 release, intracellular IL-10 expression, p-ERK1/2 expression and CB2 expression, while AM251 (CB1 antagonist) failed to. Data were presented as mean ± SEM. *p < 0.05 and **p < 0.01 versus control group, ##p < 0.01 versus THC group.