Fig. 5

VDBP overexpression weakened LPS-induced THLE2 liver cell injury. a THLE2 cells were treated with 1 μg/ml of LPS. At 0, 6, 12, 24, and 48 h after LPS stimulation, the cell viability was estimated by the MTT assay. Compared with 0 h group, ***P < 0.001. b THLE2 cells were stimulated with different concentrations of LPS for 24 h and then the cell viability was determined by the MTT assay. Compared with 0 ng/ml group, *P < 0.05 and ***P < 0.001. c The THLE2 cells were treated with or without 1 μg/ml of LPS for 24 h. The VDBP mRNA and protein expression levels were measured by RT-qPCR and Western blotting, respectively. The VDBP secretion level was detected by using a commercial kit. Compared with control group, ***P < 0.001. d–f THLE2 cells infected with recombinant lentiviruses encoding the human VDBP (LV-VDBP) and control (LV-NC) were treated with 1 μg/ml of LPS for 24 h, followed by the detection of cell viability, cell apoptotic rate, caspase-3 activity, caspase-9 activity, ALT, AST, MPO activity, MDA level, and GSH level. Compared with control group, ***P < 0.001; compared with LPS + LV-NC group, ^#P < 0.05, ^##P < 0.01, ^###P < 0.001. g THLE2 cells infected with LV-NC or LV-VDBP were treated with 1 μg/ml of LPS for 24 h. The protein levels of p-JNK and JNK were determined by Western blotting. ALT alanine aminotransferase, AST aspartate transaminase, GSH glutathione, JNK c-Jun N-terminal kinase, LPS lipopolysaccharide, MDA malondialdehyde, MPO myeloperoxidase, p-JNK phosphorylated JNK, VDBP vitamin D binding protein