Clinical laboratory · 2019
MiR-218-XOR-ROS Pathway Regulates the Progression of Nonalcoholic Steatohepatitis.
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He Junling, Zhang Juanwen, Yu Mosang, Huang Yue, Dai Yuying, Zheng Ruoheng
Аннотация
BACKGROUND: To investigate the role of the miR-218-xanthine oxidoreductase (XOR) pathway in the pathogenesis of nonalcoholic steatohepatitis (NASH) and to explore the potential downstream mechanisms involving oxidative stress and energy metabolism.
METHODS: The NASH animal model was established by feeding BALB/c mice with an MCD diet, while BRL-3A cells were cultured with a mixture of oleate and palmitate for 72 hours to mimic the steatosis and inflammation of NASH in vitro. The steatosis and inflammation levels were assessed by H-E/oil-red staining and serum/supernatant TG, ALT, and AST levels. The apoptosis degree was tested by the TUNEL/flow cytometry method both in animals and cultured cells. The XOR and miR-218 levels were detected by western blotting and qRT-PCR.
RESULTS: Decreased miR-218 and increased XOR levels were identified in the NASH animal and cell models, while the regulation of miR-218 on XOR was also confirmed. NASH alleviation was achieved after miR-218 over-expression in vivo and in vitro, according to the declination of steatosis and inflammation-related markers. Although H2O2 and ATP levels were increased and decreased in NASH models, respectively, antagonizing miR-218 could significantly alleviate those changes.
CONCLUSIONS: The miR-218-XOR pathway may provide a novel mechanism and treatment option for NASH.
METHODS: The NASH animal model was established by feeding BALB/c mice with an MCD diet, while BRL-3A cells were cultured with a mixture of oleate and palmitate for 72 hours to mimic the steatosis and inflammation of NASH in vitro. The steatosis and inflammation levels were assessed by H-E/oil-red staining and serum/supernatant TG, ALT, and AST levels. The apoptosis degree was tested by the TUNEL/flow cytometry method both in animals and cultured cells. The XOR and miR-218 levels were detected by western blotting and qRT-PCR.
RESULTS: Decreased miR-218 and increased XOR levels were identified in the NASH animal and cell models, while the regulation of miR-218 on XOR was also confirmed. NASH alleviation was achieved after miR-218 over-expression in vivo and in vitro, according to the declination of steatosis and inflammation-related markers. Although H2O2 and ATP levels were increased and decreased in NASH models, respectively, antagonizing miR-218 could significantly alleviate those changes.
CONCLUSIONS: The miR-218-XOR pathway may provide a novel mechanism and treatment option for NASH.
Предметные рубрики MeSH
3' Untranslated RegionsAnimalsBase SequenceCell LineDisease Models, AnimalDisease ProgressionGene Expression RegulationHEK293 CellsHumansMaleMiceMice, Inbred BALB CMicroRNAsNon-alcoholic Fatty Liver DiseaseRNA InterferenceReactive Oxygen SpeciesSequence Homology, Nucleic AcidSignal TransductionXanthine Dehydrogenase