Small molecules facilitate single factor-mediated sweat gland cell reprogramming.

Background: Large skin defects severely disrupt the overall skin structure and can irreversibly damage sweat glands (SG), thus impairing the skin's physiological function. This study aims to develop a stepwise reprogramming strategy to convert fibroblasts into SG lineages, which may provide a promising method to obtain desirable cell types for the functional repair and regeneration of damaged skin.

Methods: The expression of the SG markers cytokeratin 5 (CK5), cytokeratin 10 (CK10), cytokeratin 18 (CK18), carcino-embryonic antigen (CEA), aquaporin 5 (AQP5) and α-smooth muscle actin (α-SMA) was assessed with quantitative PCR (qPCR), immunofluorescence and flow cytometry.

Astragalus Polysaccharides Reduce High-glucose-induced Rat Aortic Endothelial Cell Senescence and Inflammasome Activation by Modulating the Mitochondrial Na/Ca Exchanger.

Vascular endothelial cells play a vital role in atherosclerotic changes and the progression of cardiovascular disease in older adults. Previous studies have indicated that Astragalus polysaccharides (APS), a main active component of the traditional Chinese medicine Astragalus, protect mitochondria and exert an antiaging effect in the mouse liver and brain. However, the effect of APS on rat aortic endothelial cell (RAEC) senescence and its underlying mechanism have not been investigated.

Ginsenoside Rb1 alleviates diabetic kidney podocyte injury by inhibiting aldose reductase activity.

Panax notoginseng, a traditional Chinese medicine, exerts beneficial effect on diabetic kidney disease (DKD), but its mechanism is not well clarified. In this study we investigated the effects of ginsenoside Rb1 (Rb1), the main active ingredients of Panax notoginseng, in alleviating podocyte injury in diabetic nephropathy and the underlying mechanisms. In cultured mouse podocyte cells, Rb1 (10 μM) significantly inhibited high glucose-induced cell apoptosis and mitochondrial injury.

Modulation of Macrophage Polarization by Human Glomerular Mesangial Cells in Response to the Stimuli in Renal Microenvironment.

Mesangial cell (MC) activation and macrophage infiltration are 2 major events closely related with each other in mesangial proliferative glomerulonephritis. In the anti-Thy 1 nephritis model, macrophages mediate the damage and also the expansion of mesangium through secreting various inflammatory factors; however, in glomerular microenvironment how MCs affect macrophage activity in the presence of various stimuli have not yet been understood. In the present study, we found that resting human MCs (HMCs) constitutively expressed chemokine [C-C motif] ligand 2 (CCL-2) and interleukin (IL)-6 and induced M2 polarization of macrophages in the coculture system.

New Mutation of Coenzyme Q Monooxygenase 6 Causing Podocyte Injury in a Focal Segmental Glomerulosclerosis Patient.

Background: Focal segmental glomerulosclerosis (FSGS) is a kidney disease that is commonly associated with proteinuria and the progressive loss of renal function, which is characterized by podocyte injury and the depletion and collapse of glomerular capillary segments. The pathogenesis of FSGS has not been completely elucidated; however, recent advances in molecular genetics have provided increasing evidence that podocyte structural and functional disruption is central to FSGS pathogenesis. Here, we identified a patient with FSGS and aimed to characterize the pathogenic gene and verify its mechanism.

Alleviation of senescence and epithelial-mesenchymal transition in aging kidney by short-term caloric restriction and caloric restriction mimetics via modulation of AMPK/mTOR signaling.

Renal fibrosis contributes to declining renal function in the elderly. What is unclear however, is whether epithelial-mesenchymal transition (EMT) contributes to this age-related renal fibrosis. Here, we analyzed indicators of EMT during kidney aging and investigated the protective effects and mechanisms of short-term regimens of caloric restriction (CR) or caloric restriction mimetics (CRMs), including resveratrol and metformin.

The mitochondrial Na(+)/Ca(2+) exchanger may reduce high glucose-induced oxidative stress and nucleotide-binding oligomerization domain receptor 3 inflammasome activation in endothelial cells.

Background: The mitochondrial Na(+)/Ca(2+) exchanger, NCLX, plays an important role in the balance between Ca(2+) influx and efflux across the mitochondrial inner membrane in endothelial cells. Mitochondrial metabolism is likely to be affected by the activity of NCLX because Ca(2+) activates several enzymes of the Krebs cycle. It is currently believed that mitochondria are not only centers of energy production but are also important sites of reactive oxygen species (ROS) generation and nucleotide-binding oligomerization domain receptor 3 (NLRP3) inflammasome activation.

Effects of compound Shenhua tablet on renal tubular Na+-K+-ATPase in rats with acute ischemic reperfusion injury.

Objective: To observe the effect of Compound Shenhua Tablet (, SHT) on the sodium-potassium- exchanging adenosinetriphosphatase (Na(+)-K(+)-ATPase) in the renal tubular epithelial cells of rats with acute ischemic reperfusion and to investigate the mechanisms underlying the effects of SHT on renal ischemic reperfusion injury (RIRI).

Methods: Fifty male Wistar rats were randomly divided into the sham surgery group, model group, astragaloside group [150 mg/(kg·d)], SHT low-dose group [1.5 g/(kg·d)] and SHT high-dose group [3.

AMPK-mediated downregulation of connexin43 and premature senescence of mesangial cells under high-glucose conditions.

Diabetic nephropathy is associated with premature senescence. Our previous study showed that glomerular mesangial cells (GMCs) appeared to take on senescent phenotypes under high-glucose conditions in conjunction with the downregulation of connexin43 (Cx43). In this study, we investigated whether AMPK-mediated Cx43 expression and premature senescence in diabetic nephropathy are associated with mTOR activation.

Beneficial effects of short-term calorie restriction against cisplatin-induced acute renal injury in aged rats.

Background: The therapeutic use of the antineoplastic drug cisplatin (DDP) in the elderly is limited by its nephrotoxic effects. The aim of this study was to examine the effect of short-term calorie restriction (CR) on DDP-induced nephrotoxicity in aged rats.

Methods: A group of 25-month-old male Sprague-Dawley rats were divided into two groups: ad libitum (AL) and CR, which were fed 60% of the food consumed by AL rats for 8 weeks.

Inhibition of the tubular epithelial-to-mesenchymal transition in vivo and in vitro by the Uremic Clearance Granule ().

Objective: To investigate the effect of the Uremic Clearance Granule (UCG, ), a Chinese patent medicine, on tubular epithelial-to-mesenchymal transition (EMT) in a unilateral ureteral obstruction (UUO) model in vivo and transforming growth factor (TGF)-β1 induced EMT of HK-2 cells in vitro.

Methods: In vivo study, 50 Sprague Dawley rats were divided into three groups: a sham operation group (n=10), a UUO group (n=20), and a UUO with UCG treatment group (n=20). The UCG was given at a dose of 4.

Resveratrol attenuates left ventricular remodeling in old rats with COPD induced by cigarette smoke exposure and LPS instillation.

The objective of this study was to investigate left cardiac damage and the cardioprotective effects of resveratrol in old rats with COPD. Rats 22 months old were divided into three groups: control (CTL), smoking and lipopolysaccharides (SM/LPS), and SM/LPS plus resveratrol (SM/LPS-Res). Cardiac function, pathology, oxidative stress, and apoptosis index were measured.

Mesenchymal stem cells ameliorate sepsis-associated acute kidney injury in mice.

Objective: Significant progress has been made in critical care medicine during the past several decades. However, the mortality rate is still high in patients with sepsis, especially with acute kidney injury (AKI). Mesenchymal stem cells (MSCs) possess an ability to ameliorate renal injury from ischemia-reperfusion, but it is still unknown whether they have the ability to reduce sepsis-associated AKI.

Glycated albumin may be a choice, but not an alternative marker of glycated hemoglobin for glycemic control assessment in diabetic patients undergoing maintenance hemodialysis.

Background: It has been suggested that glycated hemoglobin (HbA1c) underestimate the actual glycemic control levels in maintenance hemodialysis (MHD) patients, because of anemia and the using of erythropoietin (EPO); it was recommended that glycated albumin (GA) should be an alternative marker. Therefore, the assessment performances of glycemic control were compared between GA and HbA1c in this research by referring to mean plasma glucose (MPG) in diabetes mellitus (DM) patients undergoing MHD or not.

Methods: MPG was calculated according to the data registered at enrollment and follow-up 2 months later and corresponding HbA1c, albumin (ALB), GA, etc.

DAP5 ameliorates cisplatin-induced apoptosis of renal tubular cells.

Background: Nephrotoxicity of cisplatin limits its clinical application. Cisplatin-induced acute renal tubular epithelial cell apoptosis is one of the major mechanisms of cisplatin nephrotoxicity. Here, the role and regulation of death-associated protein 5 (DAP5) in cisplatin-induced tubular cell apoptosis were investigated.

[Experimental study of immunological function regulated by Fufang Hongjingtian capsule in mice].

The aim of this study was to investigate the immunological function regulated by Fufang Hongjingtian capsule (HJT) in mice. The mice were given ig HJT 25, 250 and 750 mg/kg, once daily, for 30 - 38 d, respectively. The mice in control group were given ig corresponding solvent.

High glucose-induced hypertrophy of mesangial cells is reversed by connexin43 overexpression via PTEN/Akt/mTOR signaling.

Background: Hypertrophy of glomerular mesangial cells (GMC) is one of the earliest pathological abnormalities in diabetic nephropathy, which correlates with eventual glomerulosclerosis. We have previously proved that this hypertrophy is mediated by downregulation of connexin43 (Cx43) and dysfunction of gap junctional intercellular communication, but the mechanism involved is still unclear. This study aims to investigate whether PTEN/Akt/mammalian target of rapamycin (mTOR) was involved as the downstream molecular signaling of Cx43 in regulating high glucose-induced GMC hypertrophy.

[Protective effects of compound tianpupian against oxidative damage in mouse erythrocytes].

The aim of this study was to investigate the protective effects of compound tianpupian (TPP) and its compositions against oxidative damage in mouse erythrocytes. The protective effect of TPP and its compositions against the red cell hemolysis induced by (2)O(2) or auto-oxidation were observed by scanning electron microscopy and spectrophotomety. The result indicated that compound TPP and all of its four components including extract of Rhodiola sachalinensis, Grape Seed Extract proanthocyanidins, Acanthopanax senticosus extract, and tea polyphenols had significant inhibitory activities for the oxidative damage of mouse erythrocytes, out of which the Grape seed extract proanthocyanidins showed the maximal protective effect.

Grape seed extract enhances eNOS expression and NO production through regulating calcium-mediated AKT phosphorylation in H2O2-treated endothelium.

GSE (grape seed extract) has been shown to exhibit protective effects against cardiovascular events and atherosclerosis, although the underlying molecular mechanisms of action are unknown. Herein, we assessed the ability of GSE to enhance eNOS (endothelial nitric oxide synthase) expression and NO (nitric oxide) production in H2O2 (hydrogen peroxide)-treated HUVECs (human umbilical vein endothelial cells). GSE enhanced eNOS expression and NO release in H2O2-treated cells in a dose-dependent manner.