糖尿病肾病
PI3K/AKT/mTOR通路
炎症
细胞凋亡
蛋白激酶B
小RNA
癌症研究
肾病
医学
内科学
内分泌学
化学
糖尿病
生物化学
基因
作者
Zhe Lou,Qiaobei Li,Chunyan Wang,Yinyan Li
标识
DOI:10.1080/13813455.2020.1767146
摘要
Gene expression microarray and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to measure the expression of miR-126. In model of diabetic nephropathy, we demonstrated that miR-126 expression was down-regulated, compared with control group. Down-expression of miR-126 promoted cell apoptosis and increased inflammation (as indicated by the levels of IL-1β, IL-6, IL-18 and TNF-α) of diabetic nephropathy in vitro. miR-126 over-expression led to significant inhibition of cell apoptosis and suppressed inflammation (IL-1β, IL-6, IL-18 and TNF-α). However, the down-expression of miR-126 suppressed the protein expression of VEGF, PI3K and p-AKT in diabetic nephropathy in vitro. On the contrary, over-expression of miR-126 induced the protein expression of VEGF, PI3K and p-AKT in diabetic nephropathy in vitro. The inhibition of VEGF increased the effect of miR-126 down-expression on apoptosis and inflammation in diabetic nephropathy in vitro. We investigated the specific function of miR-126 in patients with diabetic nephropathy and its possible mechanism.
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