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miR-548ag通过激活TLR(7/8) /NF-κB通路,促进肝细胞中的DPP4表达

Jianyu Xiong¹, Chaoyue Sun^1,2, Xin Wen^1,2

¹Medical College of Shihezi University, Bei-Er-Lu, Shihezi, 832000, Xinjiang, China.

International journal of obesity (2005)

|February 29, 2024

概括

肥胖增加了miR-548ag,它通过TLR7 / 8 / NF-κB通路升高调节二基酶-4 (DPP4),恶化了2型糖尿病 (T2DM). 抑制miR-548ag可以改善葡萄糖耐受性和胰岛素敏感性.

科学领域:

分子生物学分子生物学
内分泌学在内分泌学.
免疫学免疫学免疫学

背景情况:

肥胖与miR-548ag的增加有关,这促进了2型糖尿病 (T2DM) 通过在肝脏上调调节二乙酶-4 (DPP4).
目前尚不完全了解miR-548ag增强DPP4表达的确切分子机制.

研究的目的:

研究miR-548ag通过哪些分子机制在肝细胞中调高DPP4表达.
为了测试miR-548ag激活TLR(7/8) /NF-κB信号通路以增加DPP4表达的假设.

主要方法:

使用小鼠模型 (C57BL/6J,db/db),涉及高脂肪饮食和miR-548ag模仿剂或抑制剂的使用.
使用定量实时PCR (qRT-PCR) 和西部Blot来评估miR-548ag,DPP4和TLR7/8) /NF-κB通路的激活.
在体外研究中,利用HepG2和L02细胞与miR-548ag模仿,抑制剂和TLR7/8干扰片段进行传染.

主要成果:

在肥胖小鼠中观察到升高的miR-548ag,TLR7/8和DPP4表达.
发现miR-548ag通过TLR(7/8) /NF-κB通路促进肝细胞中的DPP4表达,减少肝细胞的葡萄糖消耗.
服用miR-548ag抑制剂改善了db/db小鼠的葡萄糖耐受性和胰岛素敏感性.

结论:

miR-548ag通过激活TLR(7/8) /NF-κB信号通路,促进肝细胞中的DPP4表达.
miR-548ag代表了管理T2DM的潜在治疗标.

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