Abstract
The present study aims to probe the impact of mesenchymal stem cells (MSCs) on the HMGA2 gene and renal tubular epithelial cell EMT in diabetic nephropathy (DN). The advanced glycation end product (AGE) in the later period was used to interfere with the HK-2 cell modeling of humans in vitro, while STZ was used for the modeling of mice DN in vivo. Allogeneic MSCs were used to interfere with the model to detect the concentration of the correlation factor in cells and mice kidney tissues and HMGA2 expression level. The following aspects were prompted after treatment with MSCs in vitro and in vivo: (1) TGF-β1 concentration, Smad2, HMGA2, vimentin and α-SMA expression levels were significantly reduced, when compared to the model group (P <0.05), while Smad7 and E-cadherin expression levels significantly increased, when compared to the model group (P <0.05); (2) The proteinuria and serum creatinine level of mice were alleviated, and the ultrastructure damage condition of kidneys also improved, when compared to the model group. MSCs can restrain the high expression of HMGA2 in DN, EMT and kidney fibrosis, and postpone renal function progression.
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