Aloperin improves liver non-alcoholic steatohepatitis in vitro and in vivo.

INTRODUCTION

The aim of this work is to investigate the inhibitory effect of aloperin (Alo) on hepatocyte apoptosis in non-alcoholic fatty liver disease, and the underlying mechanism.

MATERIAL AND

METHODS

Rats in the Alo groups were fed a high-fat + high-sugar diet for 8 weeks and then treated with low-, moderate-, and high-dose Alo for another 8 weeks via gavage. Oxidative stress indices were tested by a colourimetric method, and pathological changes were observed by haematoxylin-eosin staining. Apoptosis was detected by TUNEL staining. TLR4, TRIF, and NF-κB(p65) mRNA and protein expressions were detected by RT-qPCR, Western blot assay and immunohistochemistry. In the in vitro study, L02 cells were treated with FFA (free fatty acid) for 24 h to establish a non-alcoholic steatohepatitis (NASH) model. Inhibition of cell proliferation was measured by the MTT method, and cell apoptosis was evaluated by flow cytometry. Finally, the nuclear import volume of NF-κB(p65) was evaluated by cellular immunofluorescence.

RESULTS

Cell apoptosis significantly decreased in the Alo-treatment groups in a dose-dependent manner (p < 0.05). TLR4, TRIF, and NF-κB(p65) expression in the Alo-treatment groups was significantly downregulated compared with model group (p < 0.05). The cell proliferation rate significantly increased, cell apoptosis significantly decreased (p < 0.05), and the TLR4/TRIF/NF-κB pathway was significantly inhibited (p < 0.05) in the Alo-treatment groups. The nuclear import volume of NF-κB(p65) in the Alo-treatment groups was significantly decreased compared with that in the model group in a dose-dependent manger (p < 0.05).

CONCLUSIONS

Alo could improve NASH via the TLR4/TRIF/NF-κB pathway.