[Lithium chloride arrests HK-2 cell cycle in G2 phase through AKT/GSK-3β signal pathway].

Objective: To investigate the effect of lithium chloride (LiCl) on cell cycle of HK-2 cells and explore the possible pathways involved.

Methods: HK-2 cells were treated with LiCl at different concentrations (5, 12.5, 20, and 25 mmol/L) for 12, 24, 48, or 72 h, and the changes in cell cycle and viability were detected using flow cytometry and CCK-8 assay, respectively.

[P38 MAPK signaling pathway mediates advanced oxidation protein product-induced epithelial-to-mesenchymal transition in tubular cells].

Objective: To investigate whether the p38 mitogen-activated protein kinase (MAPK) signaling pathway mediates advanced oxidation protein products (AOPPs)-induced epithelial-to-mesenchymal transition (EMT) in tubular cells.

Methods: Human proximal tubular cells (HK-2 cells) exposed to AOPP-bovine serum albumin (BSA) were examined for expressions of p38 MAPK and phosphorylated p38 MAPK using Western blotting. Western blotting and quantitative RT-PCR were used to examine the protein and mRNA expressions of EMT markers E-cadherin and vimentin and endoplasmic reticulum stress marker glucose-regulated protein (GRP) 78 in cells treated with SB203580 (an inhibitor of the p38 MAPK signaling pathway) prior to AOPP exposure.

[Arctiin ameliorates advanced oxidation protein product-induced epithelial-to- mesenchymal transition in HK-2 cells by inhibiting endoplasmic reticulum stress].

Objective: To investigate the effect of arctiin on advanced oxidation protein product (AOPP)-induced epithelial-to-mesenchymal transition (EMT) in tubular cells and explore the mechanisms underlying this effect.

Methods: Human proximal tubular cells (HK-2 cells) were treated with bovine serum albumin (BSA) or AOPPs in the presence or absence of arctiin. The expressions of E-cadherin, vimentin, and GRP78 at the protein and mRNA levels in the cells were examined using Western blotting and quantitative real-time PCR.