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miR-122和miR-33在人体胆固醇代谢中起着关键的作用。miR-122主要受miR-370的调控。当细胞内miR-370过表达时,miR-122的表达也会相应增加。各项研究表明,miR-122的表达增加后,人体内胆固醇的含量也会相应增加;当使用抗miR-122沉默miR-122基因来抑制miR-122的表达时,胆固醇的含量就会下降。miR-33a是位于人类srebp2上的内含子miRNA。与miR-122作用相反,miR-33对人体胆固醇的代谢起着负调控的作用,这种负调控作用是通过miR-33对ATP结合盒转运子A1(ABCA1)、ABCG1和NPC1三个靶基因的结合来实现的。
miR-122 and miR-33 play key roles in human cholesterol metabolism. miR-122 is mainly regulated by miR-370. When miR-370 is overexpressed in the cell, the expression of miR-122 is also increased accordingly. Various studies have shown that, after the expression of miR-122 is increased, the content of cholesterol in the human body will also increase correspondingly; when the anti-miR-122 silencing miR-122 gene is used to inhibit the expression of miR-122, the cholesterol content will be decreased. miR-33a is an intron miRNA located on human srebp2. In contrast to the role of miR-122, miR-33 plays a negative regulative role in the metabolism of human cholesterol, which is mediated by miR-33 on the ATP binding cassette transporter A1 (ABCA1), ABCG1 and NPC1 target genes The combination of to achieve.