EXPERIMENTAL RESEARCH
Aloperin improves liver non-alcoholic steatohepatitis in vitro and in vivo
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Department of Infection Diseases and Liver Diseases, The First Affiliated Hospital of Shandong First Medical University (Shandong Provincial Qianfoshan Hospital), Jinan, China
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Department of Hepatology, Beijing Ditan Hospital Capital Medical University, Beijing, China
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PCR laboratory,The First Affiliated Hospital of Shandong First Medical University (Shandong Provincial Qianfoshan Hospital), Jinan, China
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Department of Clinical Pathology, The First Affiliated Hospital of Shandong First Medical University (Shandong Provincial Qianfoshan Hospital), Jinan, China
Submission date: 2020-01-06
Final revision date: 2020-01-31
Acceptance date: 2020-02-06
Online publication date: 2020-05-25
 
 
KEYWORDS
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ABSTRACT
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 eight weeks and then treated with low-, moderate-, and high-dose Alo for another eight 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-B(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-B(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-B(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-B pathway was significantly inhibited (p < 0.05) in the Alo-treatment groups. The nuclear import volume of NF-B(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-B pathway.

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ISSN:1734-1922