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Updated: May 15, 2025
Incorporation of a Survivable Liver Biopsy Procedure in Mice to Assess Non-alcoholic Steatohepatitis NASH Resolution
Published on: April 16, 2019
Aloperin improves liver non-alcoholic steatohepatitis in vitro and in vivo
Zhongsheng Guo1, Ruyu Liu2, Liwei Guo1
1Department of Infection Diseases and Liver Diseases, The First Affiliated Hospital of Shandong First Medical University (Shandong Provincial Qianfoshan Hospital), Jinan, China.
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.
