Influence of LncRNA UCA1 on glucose metabolism in rats with diabetic nephropathy through PI3K-Akt signaling pathway.

Abstract

The aim of this study was to investigate the influence of long non-coding ribonucleic acid (lncRNA) urothelial carcinoma associated 1 (UCA1) on glucose metabolism in rats with diabetic nephropathy (DN), and to explore its regulatory mechanism. A total of 30 healthy Sprague-Dawley (SD) rats were selected in this study. All rats were randomly divided into three groups, including the control group, the model group, and the lncRNA UCA1 inhibitor group. The rat model of DN was successfully established via intraperitoneal injection of streptozotocin (STZ). The pathological changes in kidney tissues were detected via hematoxylin-eosin (HE) staining. The levels of blood urea nitrogen (BUN), serum creatinine (Scr), and urinary protein (UP) were detected using the biochemical method. Meanwhile, the content of serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) was detected via enzyme-linked immunosorbent assay (ELISA). In addition, the messenger RNA (mRNA) and protein levels of phosphatidylinositol 3-hydroxy kinase (PI3K) and protein kinase B (Akt) in kidney tissues were detected via reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, respectively. The model group showed severe pathological damage to the kidney, compared with the control group. Meanwhile, the levels of BUN, Scr and UP, and the content of serum TNF-α and IL-6 increased significantly in the model group. The mRNA and the protein levels of PI3K and Akt in kidney tissues of the model group were significantly up-regulated as well. LncRNA UCA1 inhibitor group exhibited relieved pathological damage to the kidney, compared with the model group. The levels of BUN, Scr and UP, and the content of serum TNF-α and IL-6 remarkably decreased in UCA1 inhibitor group. Furthermore, the mRNA and the protein levels of PI3K and Akt in kidney tissues of UCA1 inhibitor groups were significantly down-regulated. LncRNA UCA1 can relieve the pathological damage to the kidney, improve renal function, and alleviate inflammatory response in DN rats. The underlying mechanism may be related to the inhibition of the PI3K-Akt signaling pathway.