Skip to main content

Advertisement

Fig. 8 | Journal of Neuroinflammation

Fig. 8

From: Benefits of VCE-003.2, a cannabigerol quinone derivative, against inflammation-driven neuronal deterioration in experimental Parkinson’s disease: possible involvement of different binding sites at the PPARγ receptor

Fig. 8

Effects of T0070907 on RGZ- and VCE-003.2-induced PPARγ transcriptional activity and MSCs differentiation. HEK-293T cells were transiently transfected with PPARγ-GAL4 plus GAL4-luc, pre-incubated with T0070907 (5 μM) for 15 min and then treated with increasing concentrations of either RGZ (a) or VCE-003.2 (b) for 6 h and luciferase activity measured in the cell lysates (open circles, PPARγ ligand; dark circles, PPARγ ligand plus T0070907). c Cells were transfected with the same pair of plasmids and treated with RGZ, VCE-003.2, or a combination of both compounds for 6 h and luciferase activity measured in the cell lysates. T0070907 prevented d RGZ- and e VCE-003.2-induced adipogenic differentiation in MSCs. The cells were differentiated in AM in the presence of RGZ and VCE-003.2 in the absence and the presence of T0070907, and adipogenic markers were characterized. Gene expression of adipogenic markers such as PPARγ2, LPL, FABP4, CEBPA, and ADIPOQ were measured after 7 days of differentiation. Data were assessed by the one-way analysis of variance followed by the Tukey test (*p < 0.05, **p < 0.01, ***p < 0.001 RGZ or VCE-003.2 compared to the control cells; ##p < 0.01, ###p < 0.001 RGZ or VCE-003.2 + T0070907 compared to RGZ- or VCE-003.2-treated cells)

Back to article page