miR-122 抑制可减轻非酒精性脂肪性肝病细胞模型中的脂质积累和炎症反应。
The miR-122 inhibition alleviates lipid accumulation and inflammation in NAFLD cell model.
机构信息
Department of Gastroenterology, Shunde Hospital of Southern Medical University, Foshan, China.
Department of Infectious Diseases, Shunde Hospital of Southern Medical University, Foshan, China.
出版信息
Arch Physiol Biochem. 2021 Oct;127(5):385-389. doi: 10.1080/13813455.2019.1640744. Epub 2019 Jul 16.
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.
背景
越来越多的证据表明，miR-122 在非酒精性脂肪性肝病（NAFLD）患者中的表达异常；然而，miR-122 在 NAFLD 中对脂质积累和炎症的作用尚不清楚。
方法
采用 RT-qPCR 检测转染 miR-122 抑制剂或用油酸（OA）处理后 miR-122 和促炎细胞因子的表达水平。通过甘油三酯含量试验和油红 O 染色检测脂质积累。采用 Western blot 检测 TLR7、TLR4、MyD88 和 NF-κBp65 的蛋白水平。
结果
我们发现 OA 促进了脂质积累和促炎细胞因子的分泌，并激活了 TLR4/MyD88/NF-κBp65 信号通路，而转染 miR-122 抑制剂后则恢复了该信号通路。
结论
这些结果表明，miR-122 抑制可减轻 OA 诱导的 L02 细胞中的脂质积累和炎症，可能通过抑制 TLR4/MyD88/NF-κBp65 信号通路。miR-122 抑制在 NAFLD 中的保护机制有待进一步研究。
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