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. 2017 May 4;8(39):64853–64866. doi: 10.18632/oncotarget.17614

Figure 8. Activation of Stat3 through the phosphorylation of Akt and Erk1/2 was required for CB2 agonist-elicited beneficial actions in AD-MSCs.

Figure 8

A. Representative photographs of immune blot of Akt, Erk, Stat3 and their phosphorylation. (n = 3), B.-D. Quantitative analysis of A.. *P < 0.05 between indicated groups. AD-MSCs were pre-treated with CB2 agonist (5 μM, 12 h) in the presence or absence of AM630 (4μM, a CB2 inhibitor), U0126 (5μM, an Erk1/2 inhibitor), LY294002 (5μM, a PI3K/Akt inhibitor) or AG490 (a Stat3 inhibitor, 40μM) and subsequently underwent H2O2/SD insult. E. Paracrine growth factor VEGF secreted by AD-MSCs following indicated treatment, F. LDH release by AD-MSCs after indicated treatment, n = 3. G. Flow cytometry analysis of ROS production in AD-MSCs after indicated treatment, n = 3. n = 3. *P < 0.05 versus blank control, #P < 0.05 versus H2O2/SD, †P < 0.05 versus H2O2/SD+CB2R or CB2R.