Eur Rev Med Pharmacol Sci 2019; 23 (23): 10482-10488
DOI: 10.26355/eurrev_201912_19687

Regulatory mechanism of TGF-β1/SGK1 pathway in tubulointerstitial fibrosis of diabetic nephropathy

X.-J. Miao, T.-T. Bi, J-.M. Tang, R. Lv, D.-K. Gui, X.-F. Yang

Department of Geriatrics, The First People’s Hospital of Wujiang District Suzhou, Suzhou, China. yangxufeng2012@163.com


OBJECTIVE: The aim of this study was to clarify the potential function of transforming growth factor-β1/serum/glucocorticoid-regulated kinase 1 (TGF-β1/SGK1) pathway in diabetic nephropathy-induced tubulointerstitial fibrosis.

MATERIALS AND METHODS: Type 2 diabetes mellitus (T2DM) model was successfully established in rats by high-sucrose-high-fat diet combined with streptozotocin (STZ) induction. Subsequently, blood glucose level, renal function and pathological changes in kidneys of T2DM and control rats were evaluated. Western blot and quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) were conducted to determine the protein and mRNA expression levels of TGF-β1, SGK1, fibronectin (FN) and α-smooth muscle actin (α-SMA) in rat kidney tissues, respectively.

RESULTS: Blood glucose (BG), glycosylated hemoglobin (GHb), serum creatinine (Scr) and blood urea nitrogen (BUN) in T2DM rats were significantly higher than those of control rats (p<0.05). The morphology of glomeruli and renal tubules in rats of control group were normal. In contrast, T2DM rats showed significant lesions in glomeruli, renal tubules, and renal interstitium. Furthermore, the relative expression levels of TGF-β1, SGK1, FN, and α-SMA in kidney tissues of T2DM rats were remarkably higher than those of controls (p<0.05).

CONCLUSIONS: The TGF-β1/SGK1 pathway is closely related to tubulointerstitial fibrosis in T2DM rats.

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X.-J. Miao, T.-T. Bi, J-.M. Tang, R. Lv, D.-K. Gui, X.-F. Yang
Regulatory mechanism of TGF-β1/SGK1 pathway in tubulointerstitial fibrosis of diabetic nephropathy

Eur Rev Med Pharmacol Sci
Year: 2019
Vol. 23 - N. 23
Pages: 10482-10488
DOI: 10.26355/eurrev_201912_19687