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. 2017 Oct 4;7:12671. doi: 10.1038/s41598-017-12570-6

Figure 4.

Figure 4

Effect of PPAR-γ agonist inhibits FLSs proliferation and migration. (a) Concentration-dependent inhibition expression of PPAR-γ mRNA by Pioditazone in AA FLSs, tested by Q-PCR assays. (b) The mRNA levels of PPAR-γ, c-Myc and Cyclin D1 were analyzed by Q-PCR in FLSs with Pioditazone. (c) The protein levels of PPAR-γ, c-Myc and Cyclin D1 were analyzed by Western blot in FLSs with Pioditazone. (d) The mRNA levels of MMP-3, MMP-9 and TIMP-1 were analyzed by Q-PCR in FLSs with Pioditazone. (e) The protein levels of MMP-3, MMP-9 and TIMP-1 were analyzed by Western blot in FLSs with Pioditazone. (f) Cell cycle of FLSs were incubated with Pioditazone for 48 h and then subjected to the FACS analysis. (g) After stained with CFDA-SE, FLSs were incubated with Pioditazone for six days and then subjected to the FACS analysis. (h) BrdU proliferation assay were treated with Pioditazone 48 h in FLSs. (i) FLSs were treated with Pioditazone, and migration into the wound-healing 24 h was photographed (original magnification, ×10). (j) FLSs were treated with Pioditazone, and transwell migration 48 h was photographed (original magnification, ×10). All values were expressed as mean ± SEM. #P < 0.05, ##P < 0.01 vs normal group. *P < 0.05, **P < 0.01 vs model group.