Advanced glycation end products (AGEs) are formed via nonenzymatic reactions between reducing sugars and proteins. Recent studies have shown that methylglyoxal, a potent precursor for AGEs, causes a variety of biological dysfunctions, including diabetes, inflammation, renal failure, and cancer. However, little is known about the function of methylglyoxal-derived AGEs (AGE4) in kidney cells. Therefore, we verified the expression of endoplasmic reticulum (ER) stress-related genes and apoptosis markers to determine the effects of AGE4 on human proximal epithelial cells (HK-2). Moreover, our results showed that AGE4 induced the expression of apoptosis markers, such as Bax, p53, and kidney injury molecule-1, but downregulated Bcl-2 and cyclin D1 levels. AGE4 also promoted the expression of NF-κB, serving as a transcription factor, and the phosphorylation of c-Jun NH2-terminal kinase (JNK), which induced cell apoptosis and ER stress mediated by the JNK inhibitor. Furthermore, AGE4 induced mitochondrial dysfunction by inducing the permeabilization of the mitochondrial membrane and ATP synthesis. Through in vitro and in vivo experiments, this study provides a new perspective on renal dysfunction with regard to the AGE4-induced RAGE /JNK signaling pathway, which leads to renal cell apoptosis via the imbalance of mitochondrial function and ER stress in kidney damage.

The accumulation of reactive a-dicarbonyl leading to advanced glycation end products (AGEs) have been linked to pathophysiological diseases in many studies, such as atherosclerosis, cataract, cancer, and diabetic nephropathy. Glycation-generated AGEs increase the expression of inflammatory cytokines by transferring signals to the cell by binding them to the receptor for AGEs (RAGE) on their cell surface. The effect of methylglyoxalderived AGEs (AGE-4) on the induction of matrix metalloproteinases (MMPs) in rat ordinary kidney cells (NRK-52E) was explored in this research, among other AGEs. The cell treated with 100 lg/mL AGE-4 for 24 h showed a substantial rise in MMP-2 and MMP-9 expression relative to BSA control only and other AGEs through ERK, JNK, and NF-B pathways. Our findings therefore suggest that AGE-4 expresses MMPs through the AGE-4-RAGE axis, activating MAPK signals that may contribute to dysfunction of the kidney cell.

A highly dispersed W/O emulsion of silicone oil (cyclomethicone)/water system was prepared with a nonionic surfactant. The surface and interfacial tension between the oil and water were characterized in terms of the droplet size distribution and viscosity change of the emulsion. When the dispersed phase concentration was relatively high, the viscosity of the emulsion was rapidly increased and the droplet size of the emulsion was decreased. The rheological behavior of the emulsion system showed non-Newtonian and shear thinning phenomena depending upon the content of the dispersed phase. The droplet size of the emulsion was decreased with increasing surfactant content and water concentration. The relative viscosity of the emulsion was better predicted with the Choi-Schowalter model than with the Taylor model. The value of the complex modulus increased with increasing surfactant concentration. The linear viscoelastic region was expanded with a dispersed phase concentration. According to the change in the viscosity, the behavior was classified into three distinct regions: [I] linear viscoelastic, [II] partially viscoelastic, and [III] viscous. The creep/recovery behaviors in each region were characterized.

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