Non-alcoholic fatty liver disease (NAFLD) have a high prevalence in humans in the past two decades. Here, we elucidated the functions of miR-30a-3p in the development of NAFLD and identified its potential targets. HepG-2 cells and NAFLD patients' blood samples were used in our study. Bioinformatics analysis as well as luciferase reporter assays were employed to distinguish peroxisome proliferator-activated receptor alpha (PPAR-α) as a target gene. Western blotting showed the expressions of lipid metabolic proteins and the target gene PPAR-α. Oil red O staining and triglyceride activity tested the fatty deposits after treatment with miR-30a-3p. miR-30a-3p was substantially up-regulated in NAFLD. Bioinformatics analyses showed that PPAR-α was a possible target of miR-30a-3p, linked with signaling pathways in NAFLD. PPAR-α as a novel target of miR-30a-3p, and suppression of its levels. The lipid metabolic-related proteins ACC, p-GSK-3β and FASN were up-regulated after transfecting with miR-30a-3p mimic, but the proteins CPT1, p-AMPK and UCP2 were down-regulated. miR-30a-3p inhibitor could diminish the protein manifestation of ACC, p-GSK-3β and FASN; and augment the protein manifestation of CPT1, p-AMPK and UCP2. On the contrary, overexpression of miR-30a-3p had adverse impacts on the performance of hepatocellular lipid accumulation and Triglyceride (TG) activity. Co-treatment with miR-30a-3p mimic and overexpression PPAR-α could revise the hepatic steatosis and the TG level induced by fat milk. Our findings suggest that miR-30a-3p/PPAR-α may be developed as a potential agent in NAFLD, which is enough to attenuate triglyceride accumulation and hepatic steatosis.

中文翻译：

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miR-30a-3p的抑制可减轻非酒精性脂肪肝疾病中的肝脂肪变性。

在过去的二十年中，非酒精性脂肪肝疾病（NAFLD）在人类中普遍流行。在这里，我们阐明了miR-30a-3p在NAFLD发育中的功能，并确定了其潜在的靶标。我们的研究使用了HepG-2细胞和NAFLD患者的血液样本。使用生物信息学分析以及荧光素酶报告基因分析法来区分过氧化物酶体增殖物激活受体α（PPAR-α）作为靶基因。Western blotting显示脂质代谢蛋白和靶基因PPAR-α的表达。油红O染色和甘油三酸酯活性测试了miR-30a-3p处理后的脂肪沉积。miR-30a-3p在NAFLD中显着上调。生物信息学分析表明，PPAR-α是miR-30a-3p的可能靶标，与NAFLD中的信号传导途径有关。PPAR-α作为miR-30a-3p的新型靶标及其水平的抑制。用miR-30a-3p模拟物转染后，脂质代谢相关蛋白ACC，p-GSK-3β和FASN被上调，而CPT1，p-AMPK和UCP2被下调。miR-30a-3p抑制剂可减少ACC，p-GSK-3β和FASN的蛋白质表现；并增强CPT1，p-AMPK和UCP2的蛋白质表现。相反，miR-30a-3p的过表达对肝细胞脂质蓄积和甘油三酸酯（TG）活性产生不利影响。与miR-30a-3p模拟物和过表达的PPAR-α共同处理可改善脂肪脂肪引起的肝脂肪变性和TG水平。我们的发现表明，miR-30a-3p /PPAR-α可能被开发为NAFLD的潜在药物，