Abstract

This study was to discuss the impact of Circ_0015756 on podocyte injury in diabetic nephropathy and its mechanism. After transfection of podocytes with si-NC and si-Circ_0015756, they were then exposed to normal glucose and high glucose (HG). Cell invasion and migration ability were detected by Transwell and scratch test, while cell proliferation and apoptosis were analyzed by flow cytometry, and apoptosis and anti-apoptotic protein expression were analyzed by Western blotting. Bioinformatics software and gene assay were employed to detect and verify the relationship between miR-136 and Circ_0015756. Finally, the activation state of NF-κB pathway was analyzed by Western blot. HG treatment induced podocytes injury and suppressed invasion and migration activity, accompanied by increased Circ_0015756 expression. And silencing of Circ_0015756 alleviated cell injury induced by HG treatment, while miR-136 knock down abolished Circ_0015756 silencing’ protective effect. Further, silencing of Circ_0015756 inhibited NF-κB pathways by regulating miR-136. HG environment induced upregulation of Circ_0015756 expression, while silencing of Circ_0015756 regulated the NF-κB pathway by upregulating miR-136 expression, thus alleviating podocytes injury induced by HG treatment.

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