Influence of LncRNA UCA1 on glucose metabolism in rats with diabetic nephropathy through PI3K-Akt signaling pathway
Authors: R-G Chen
W-Q Li
C-H Shi
Y Huang
Journal: European Review for Medical and Pharmacological Sciences (2019)
Discipline: PHARMACOLOGY & TOXICOLOGY
Keywords: lncRNA UCA1; glucose metabolism; diabetic nephropathy; rats; kidney tissues
Affiliations: Department of Endocrinology, The People's Hospital of Danyang, Danyang, China. .

Abstract:  Objective: 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. Materials and methods: 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. Results: 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. Conclusions: 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. 

Retracted: No

PubPeer comments:
 Figure 2. * Pink boxes: The b-actin panel looks very similar to the b-actin panel in L. Zhou et al. Eur Rev Med Pharmacol Sci doi: 10.26355 eurrev_201911_19413, https: pubpeer.com publications 7610C7DEAFE5B2F5447ED558AB664B ![file] , 
 Figure 3A: The bottom parts of the PI3K lanes look very similar to those of the b-actin lanes. In addition, the top parts appear to show some brush-stroke-like light dark stripes. Also, some of the bottom parts of the lanes look similar to lanes in Figure 4A of the above-mentioned paper by L. Zhou et al. Eur Rev Med Pharmacol Sci doi: 10.26355 eurrev_201911_19413, https: pubpeer.com publications 7610C7DEAFE5B2F5447ED558AB664B Boxes of the same color show areas that look similar. ![file] ,