Association between renal α-klotho and renal pathology among patients with chronic kidney disease.

Introduction: This study was designed to investigate whether renal α-klotho levels are associated with renal pathology. This is the first report on patients with chronic kidney disease (CKD).

Methods: We conducted a retrospective observational study.

Celastrol attenuates renal injury in 5/6 nephrectomized rats via inhibiting epithelial-mesenchymal transition and transforming growth factor-β1/Smad3 pathway.

Renal injury is an important factor in the development of chronic kidney diseases that pathologically manifested as renal fibrosis and podocyte damage. In the disease state, renal fibroblasts lead to high expression levels of α-smooth muscle actin (α-SMA), while podocytes undergo epithelial-mesenchymal transition, leading to proteinuria. Celastrol, a bioactive compound in the medicinal plant Tripterygium wilfordii, was found to delay the progression of early diabetic nephropathy and attenuate renal fibrosis in mice with unilateral ureteral obstruction.

BMSC-derived exosomes protect against kidney injury through regulating klotho in 5/6 nephrectomy rats.

Aim: The aim of this study was to investigate the renoprotective effects of exosomes derived from rat bone marrow mesenchymal stem cells (rBMSCs) in a rat model of 5/6 nephrectomy (Nx)-induced chronic kidney disease (CKD).

Methods: A rat model of 5/6 Nx-induced CKD was established using conventional method. rBMSC-derived exosomes were isolated using ultracentrifugation and characterized.

TET2 mediated demethylation is involved in the protective effect of triptolide on podocytes.

The epithelial-mesenchymal transition (EMT) is usually considered the central mechanism of podocyte injury that eventually leads to proteinuria. We used an TGF-β1 induced podocyte EMT model and an rat focal segmental glomerulosclerosis (FSGS) model to uncover the mechanism underlying the protective effect of triptolide (TP) on podocytes. We found that TP could reverse the podocyte EMT process and upregulate the expression of TET2 in the TGF-β1-induced podocyte injury model.

The protective effect of Phellinus linteus decoction on podocyte injury in the kidney of FSGS rats.

Background: This study aimed to investigate the effect of the Phellinus linteus (Mesima) decoction on podocyte injury in a rat model of focal and segmental glomerulosclerosis (FSGS) and evaluate the potential mechanisms.

Methods: FSGS resembling primary FSGS in humans was established in rats by uninephrectomy and the repeated injection of doxorubicin. The FSGS rats were randomly divided into the model group, low-dose group of P.

Bone marrow mesenchymal stem cells attenuate the progression of focal segmental glomerulosclerosis in rat models.

Background: Focal segmental glomerulosclerosis (FSGS) is the most common glomerular etiology of end-stage kidney disease (ESKD). Increasing evidence has indicated the reparative potential of mesenchymal stem cells (MSCs) in damaged diseased kidneys. However, the effect of bone marrow mesenchymal stem cells (BMSCs) on the FSGS progression remains unclear.

[Study of resveratrol suppressing TGF-beta1 induced transdifferentiation of podocytes].

Objective: To explore the effect of resveratrol on transforming growth factor-beta1 (TGF-beta1) induced transdifferentiation of podocytes.

Methods: Mouse podocytes in vitro cultured under differentiating conditions for 10 days were divided into the normal group, the model group, the high dose resveratrol group, and the low dose resveratrol group. The podocytes in the high and low dose resveratrol groups were intervened with 5 micromol/L and 2 micromol/L resveratrol respectively for 30 min.

Suppression of lipopolysaccharide-induced upregulation of toll-like receptor 4 by emodin in mouse proximal tubular epithelial cells.

The aim of this study was to investigate the effects of emodin, the major component of Rheum palmatum, on lipopolysaccharide (LPS)-induced toll-like receptor 4 (TLR4) expression in cultured mouse tubular epithelial cells (TECs). The TECs were obtained from mice and incubated with LPS and/or indicated concentrations of emodin for 24 h. Cytokeratin, α-SMA and vimentin were detected using immunohistochemistry.