Fig. 7: RAactivated AMPKα via the activation of PPAR-γ | Cell Death & Disease

Fig. 7: RAactivated AMPKα via the activation of PPAR-γ

From: Rosmarinic acid attenuates cardiac fibrosis following long-term pressure overload via AMPKα/Smad3 signaling

Fig. 7

a The expression of PPAR-γ and the quantitative results in vivo (n = 6). b Representative western blots and statistical results of PPAR-γ in CFs (n = 6). c Activation of AMPKα was blocked in the presence of GW9662 in CFs (n = 6). d The relative mRNA level of α-Sma normalized to Gapdh in the presence or absence of GW9662 in CFs (n = 6). e, f Representative immunofluorescence staining of α-SMA and statistical results (n = 6). Green represented α-SMA, nuclei was stained with DAPI (blue). g Activation of AMPKα was blocked after knockdown of PPAR-γ with siPpar-γ in CFs (n = 6). h The relative mRNA level of α-Sma normalized to Gapdh with or without siPpar-γ treatment in CFs (n = 6).Values represent the mean ± SEM. Representative images are shown in b-h from three independent experiments. *P < 0.05 vs. the corresponding control CFs within vehicle or siRNA group, #P < 0.05 vs. TGF-β-treated CFs within vehicle or shRNA group, &P < 0.05 vs. the corresponding control CFs within GW9662 or siPpar-γ group. In Figs. 7a, *P < 0.05 vs. the corresponding Sham group, #P < 0.05 vs. AB+Veh. In Figs. 7b, *P < 0.05 vs. the matched group, NS no significance

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