Why the study?
Although miR-122 expression is abnormal in NAFLD patients, its role in lipid accumulation and inflammation in NAFLD remains unclear.
Inhibition of miR-122 alleviates oleic acid-induced lipid accumulation and inflammation in L02 cells, potentially via the TLR4/MyD88/NF-κBp65 pathway.
miR-122 inhibition attenuates lipid accumulation and inflammation in NAFLD cell models; leaves open clinical relevance pending human trials.
BACKGROUND: Accumulating evidence showed that the expression of miR-122 was abnormal in NAFLD patients; however, the role of miR-122 on lipid accumulation and inflammation in NAFLD is not clear. METHODS: RT-qPCR was applied to detect the expression levels of miR-122 and pro-inflammatory cytokines following transfected with miR-122 inhibitor or treated with oleic acid (OA). Detection of lipid accumulation was performed by triglyceride content test and oil red o staining assay. Western blotting was applied to detect the protein levels of TLR7, TLR4, MyD88 and NF-κBp65. RESULTS: We found that the OA promoted lipid accumulation and pro-inflammatory cytokines secretion and activated TLR4/MyD88/NF-κBp65 signalling pathway, which were restored following transfected with miR-122 inhibitor. CONCLUSIONS: These results suggested that miR-122 inhibition alleviates lipid accumulation and inflammation in L02 cell induced by OA may through inhibiting TLR4/MyD88/NF-κBp65 signalling pathway. The protective mechanism of miR-122 inhibition in NAFLD must be explored in future studies.
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Hu et al. (2019) studied this question.
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