Autophagy was decreased in the progression of renal fibrosis in diabetic nephropathy mice (in vivo) and in high glucose-induced NRK-52E cells (rat kidney epithelial cells) (in vitro) as the expression ofLC-3I and LC-3II (indicators of autophagy) were decreased mice MiR-142-5p was unregulated and PTEN was down-regulated in kidney mice and high glucose-induced NRK-52E cells.
Supplementation with bezafibrate, a PPAR pan-agonist, improved the damage of kidney in DN mice and in high glucose-induced NRK-52E cells, following the up-regulation of PPARs and the increase of CYP4A-20-HETE.
In the current study, we investigated the effects of BBR in high glucose (HG) and hypoxia-induced apoptosis with normal rat renal tubular epithelial (NRK-52E) and human kidney proximal tubular cells (HK-2) and further explored the underlying molecular mechanism of hypoxia-inducible factor 1α (HIF-1α) in diabetic kidney disease (DKD).
Using the NRK-52E cell line cultured under high glucose condition as an <i>in vitro</i> model of diabetic nephropathy, we show that loss of PSMA6 protein expression occured independent of changes the in <i>PSMA6</i> mRNA expression.