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...
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| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Termedia Publishing House
2020-05-01
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| Series: | Archives of Medical Science |
| Subjects: | |
| Online Access: | https://www.archivesofmedicalscience.com/Aloperin-improves-liver-non-alcoholic-steatohepatitis-n-in-vitro-and-in-vivo-,118004,0,2.html |
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| Summary: | 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. |
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| ISSN: | 1734-1922 1896-9151 |