ArticleArchives of medical science : AMS2026
Shikonin treatment ameliorates lipopolysaccharide-induced acute liver failure in mice via regulating miR-106/MCL1 and miR-34a/SIRT1/TP53 signaling.
Article in Archives of medical science : AMS, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Treatment with shikonin (SKN) suppresses the expression of miR-106 and miR-34a. Furthermore, SIRT1 and MCL1 are targets of miR-34a and miR-106, respectively. In this study, we treated an animal model of acute liver failure (ALF) with a high dose (1.0 mg/kg) and low dose (0.5 mg/kg) of SKN to investigate its effect on liver functions and signaling pathways of SKN/miR-106/MCL1 and SKN/miR-34a/SIRT1/TP53. Material and methods: An ALF animal model was established and the serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed to evaluate the effects of different doses of SKN. Terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) was performed to assess hepatocyte apoptosis. Luciferase assay, RT-qPCR and Western blot analysis were performed to measure the relationship between miR-106, miR-34a, SIRT1 and MCL1. Results: In the ALF mouse models, the administration of SKN decreased the levels of ALT and AST in a dose-dependent manner, along with a significantly decreased number of apoptotic hepatocytes. SKN may protect the liver during ALF via reducing the level of inflammation. Luciferase assay showed that the co-transfection of wild-type MCL1/SIRT1 and miR-106/miR-34a significantly decreased the luciferase activity of LO2 cells, thus indicating that MCL1 and SIRT1 are targets of miR-106 and miR-34a, respectively, while SIRT1 could act as a regulator of TP53. Moreover, the expression of miR-106, miR-34a and TP53 was decreased over an increasing concentration of SKN, along with the increasing mRNA and protein levels of MCL1 and SIRT1. Conclusions: In this study, we found that SKN alleviated ALF in a dose-dependent manner via regulating the signaling pathways of SKN/miR-106/MCL1 and SKN/miR-34a/SIRT1/TP53.
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