Department of Cardiac Ultrasound, the First Affiliated Hospital of China Medical University, Shenyang, China.
Ultrasonic Diagnosis, The First Affiliated Hospital of China Medical University, Shenyang, China.
Arch Physiol Biochem. 2022 Oct;128(5):1265-1274. doi: 10.1080/13813455.2020.1767146. Epub 2020 May 25.
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 . 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 . On the contrary, over-expression of miR-126 induced the protein expression of VEGF, PI3K and p-AKT in diabetic nephropathy . The inhibition of VEGF increased the effect of miR-126 down-expression on apoptosis and inflammation in diabetic nephropathy . We investigated the specific function of miR-126 in patients with diabetic nephropathy and its possible mechanism.
采用基因表达微阵列和逆转录定量聚合酶链反应（RT-qPCR）来测量 miR-126 的表达。在糖尿病肾病模型中，与对照组相比，我们证明 miR-126 的表达下调。miR-126 的下调促进细胞凋亡并增加糖尿病肾病的炎症（由 IL-1β、IL-6、IL-18 和 TNF-α 的水平表示）。miR-126 的过表达导致细胞凋亡的显著抑制并抑制炎症（IL-1β、IL-6、IL-18 和 TNF-α）。然而，miR-126 的下调抑制了糖尿病肾病中 VEGF、PI3K 和 p-AKT 的蛋白表达。相反，miR-126 的过表达诱导了糖尿病肾病中 VEGF、PI3K 和 p-AKT 的蛋白表达。VEGF 的抑制增加了 miR-126 下调对糖尿病肾病中细胞凋亡和炎症的影响。我们研究了 miR-126 在糖尿病肾病患者中的具体功能及其可能的机制。
