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Fig. 4 | Journal of Translational Medicine

Fig. 4

From: A novel role of glutathione S-transferase A3 in inhibiting hepatic stellate cell activation and rat hepatic fibrosis

Fig. 4Fig. 4Fig. 4

GSTA3 suppressed ROS accumulation and the activation of the MAPK and GSK-3β pathways in HSCs. a WB analysis of p-GSK-3β levels. Values are presented as the mean ± SD of three independent experiments. *P < 0.05 compared with the control group and #P < 0.05 compared with the PDGF-BB treatment group. b Flow cytometry was used to detect ROS accumulation in HSCs. HSCs were stimulated with PDGF-BB (10 ng/ml) for 30 min after transfection with the GSTA3 siRNA for 48 h. c, d WB analysis of p-P38, p-ERK, p-JNK and p-GSK-3β levels in CFSC-2G and LX2 cells. After an incubation with the GSTA3 siRNA-Lipofectamine 2000 complex for 6 h, HSCs were maintained in culture medium for 48 h and then stimulated with PDGF-BB (10 ng/ml) for 15 min before harvest for the protein analysis. e WB analysis of p-P38, p-ERK, p-JNK and p-GSK-3β levels in CFSC-2G cells. After an incubation with the GSTA3 plasmid-Lipofectamine 2000 complex for 6 h, HSCs were maintained in culture medium for 48 h and then stimulated with PDGF-BB (10 ng/ml) for 15 min before harvest for the protein analysis. The phosphorylation of ERK1/2, P38 and JNK were determined by calculating the ratios to the total ERK1/2, total P38 and total JNK levels, respectively. The level of the p-GSK-3β protein was normalized to GAPDH. Values are presented as the mean ± SD of three independent experiments. *P < 0.05 compared with the Si-Con group or pc-DNA3.1(+) group, # P < 0.05 compared with the Si-Con + PDGF-BB group or pc-DNA3.1(+)+PDGF-BB group, and $P < 0.05 compared with the Si-rGSTA3 + PDGF-BB or Si-hGSTA3 + PDGF-BB group

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