Fig. 2

Simvastatin deactivates HSC via LSEC and recruits NKT cells. A Quantitative RT-PCR analysis and B immunoblotting of KLF2 and eNOS in SK-Hep1 LSEC cells treated with the indicated concentrations of simvastatin for 24 h (n = 3). GAPDH acts as the loading control. C Extracellular concentration of NO upon different doses of simvastatin treatment (n = 3). D Quantitative RT-PCR analysis and, E immunoblotting of ACTA2 and COL1 in LPS-activated LX2 treated with the supernatant of SK-Hep1 upon different doses of simvastatin treatment with or without L-NAME (n = 3). GAPDH acts as the loading control. F Gene expression profiles of chemokines analyzed with RNA-seq data which derived from SK-Hep1 cells treated with simvastatin or control. Simvastatin-responsive chemokine genes were grouped in association with clusters of various immune cell-regulating functions. The p value of each comparison was indicated with colors. G Quantitative RT-PCR analysis and H immunoblotting of CXCL16 in SK-Hep1 cells treated with the indicated concentrations of simvastatin for 24 h (n = 3). GAPDH acts as the loading control. I CXCR6 expression was detected in NKT cells. J The expression of CD69 and IFN-γ was detected in NKT cells treated with control, simvastatin, the co-culture with SK-Hep1 cells, and the combination, respectively (n = 3). *p < 0.05, **p < 0.01, ***p < 0.001, n.s. = not significant