Abstract
Diabetic nephropathy is a common complication of type 2 diabetes and is related to the epithelial to mesenchymal transition. In this study, we aimed to find whether the RhoA/ROCK pathway affects the development of diabetic nephropathy caused by the epithelial to mesenchymal transition both in vivo and in vitro. The results show that inhibition of the RhoA/ROCK signaling pathway improved the pathology and degree of fibrosis in diabetic nephropathy as determined by hematoxylin and eosin staining and Masson staining. We also found, using immunohistochemistry and quantitative reverse transcription polymerase chain reaction, that a RhoA/Rock inhibitor regulated relative protein and gene expression levels in a dose-dependent manner. Furthermore, the inhibitor improved fibrosis induced by high levels of glucose in HK-2 cells by suppressing E-cadherin, α-SMA, and FSP-1 expression. In conclusion, the RhoA/ROCK signaling pathway plays an important role in the development of diabetic nephropathy and could be a potential therapeutic target for type 2 diabetes.