ABSTRACT
The development of safe and cost-effective methods for the treatment of dye polluted wastewater has been a great concern among researchers. Herein, we developed a nanocomposite (M3D-PAA-CCN) based on polyacrylic acid (PAA) crosslinked with magnetic 3D crosslinkers (M3D) and carboxylated cellulose nanocrystals (CCN), for the removal of cationic dyes from aqueous solutions. Acrylic-functionalized Fe3O4 nanoparticles were covalently linked to the polymer chains via the form of the 3D crosslinker to introduce magnetic properties into the as-synthesized nanocomposite. The addition of highly dispersive CCN reduced the gel-like properties of the nanocomposite and instead incorporated a diffusive nature, which was more desirable for adsorbents. The surface morphology of the nanocomposite was analyzed by FESEM and the size of the nanocomposite particles was found to be in the range of 60-90 nm. The chemical functionalities and compositions were determined by XPS, FTIR, and EDX analyses whereas TGA confirmed the thermal stability of M3D-PAA-CCN. The maximum adsorption capacity of the M3D-PAA-CCN (332 mg g-1) was measured higher than that of M3D-PAA (114 mg g-1) to a cationic methylene blue (MB) dye indicating the significant contribution of CCN. The adsorption capacity of the as-synthesized M3D-PAA-CCN was found to be highly pH-dependent and the adsorption capacity increased with the increase of pH owing to the greater negative charge as indicated by the higher zeta potential. The adsorption kinetics of MB on the composites was found to follow the pseudo-second-order model. The adsorption capacity was also investigated as a function of concentration to figure out the adsorption mechanism using Langmuir and Freundlich isotherm models. The Langmuir model fitted the adsorption process better as suggested by the relatively smaller nonlinear chi-square value obtained from the fitting parameters.
ABSTRACT
BACKGROUND: In observational studies, higher uric acid levels are associated with metabolic syndrome, diabetes, and kidney disease. OBJECTIVE: The objective of this study is to examine whether reduction of plasma uric acid with febuxostat, a xanthine oxido reductase inhibitor, impacts adipose tissue oxidative stress, adipokines, and markers of systemic inflammation or kidney fibrosis. DESIGN: This was a double-blinded randomized controlled trial. SETTING: Academic university setting was used. PATIENTS: Overweight or obese adults with hyperuricemia and type 2 diabetic nephropathy were included. MEASUREMENTS: Adipose tissue thiobarbituric acid reducing substances (TBARS) and adiponectin concentrations and urinary transforming growth factor-ß (TGF-ß) were primary endpoints. Plasma C-reactive protein, high molecular weight-adiponectin, interleukin-6, tumor necrosis factor-α, and TBARS and albuminuria were among predefined secondary endpoints. METHODS: Participants were randomly assigned to febuxostat (n = 40) or matching placebo (n = 40) and followed for 24 weeks. RESULTS: Baseline plasma uric acid levels were 426 ± 83 µmol/L; 95% completed the study. Estimated glomerular filtration rate (eGFR) declined from 54 ± 17 mL/min/1.73 m2 at baseline to 51 ± 17 mL/min/1.73 m2 at 24 weeks (P = .05). In separate mixed-effects models, compared with placebo, febuxostat reduced uric acid by 50% (P < .001) but had no significant effects on subcutaneous adipose tissue TBARS (-7.4%, 95% confidence interval [CI], 57.4%-101.4%) or adiponectin (6.7%, 95% CI, 26.0%-53.8%) levels or urinary TGF-ß/creatinine ratio (18.0%, 95% CI, 10.0%-54.8%) or secondary endpoints. LIMITATIONS: Relatively modest sample size and short duration of follow-up. CONCLUSIONS: In this population with progressive diabetic nephropathy, febuxostat effectively reduced plasma uric acid. However, no detectable effects were observed for the prespecified primary or secondary endpoints. TRIAL REGISTRATION: The study was registered in clinicaltrials.gov (NCT01350388).
MISE EN CONTEXTE: Dans les études observationnelles, des taux élevés d'acide urique sont associés à un syndrome métabolique, au diabète et à l'insuffisance rénale. OBJECTIFS DE L'ÉTUDE: Cette étude visait à déterminer si l'utilisation de febuxostat, un inhibiteur de la xanthine oxydoréductase, pour réduire le taux d'acide urique dans le plasma avait une incidence sur le stress oxydatif du tissu adipeux, les adipokines, les marqueurs de l'inflammation systémique ou sur la fibrose kystique. TYPE D'ÉTUDE: Il s'agit d'un essai à double insu, randomisé et contrôlé. CADRE: L'étude s'est effectuée en contexte universitaire. PATIENTS: Les participants à cette étude étaient des adultes obèses ou en surpoids, présentant une hyperuricémie ainsi qu'une néphropathie diabétique de type 2. MESURES: Les critères principaux incluaient la concentration d'adiponectine et de substances réagissant avec l'acide thiobarbiturique (TBARS) dans les tissus adipeux, de même que le facteur de croissance transformant urinaire (TGF-ß). Les critères secondaires incluaient les protéines C-réactives du plasma, l'adiponectine de poids moléculaire élevé, l'interleukine-6, le facteur de nécrose tumorale alpha, les TBARS ainsi que l'albuminurie. MÉTHODOLOGIE: On a prescrit, de façon aléatoire, du febuxostat (n = 40) ou un placebo (n = 40) aux participants, et ces derniers ont été suivis sur une période de 24 semaines. RÉSULTATS: Les valeurs initiales d'acide urique dans le plasma se situaient à 426 ± 83 µmol/L. La grande majorité des participants (95%) a complété l'étude. Le débit de filtration glomérulaire estimé a chuté de 54 ± 17 mL/min/1,73 m2, sa valeur moyenne au début de l'étude, à 51 ± 17 mL/min/1,73 m2 au bout des 24 semaines (P = 0,05). Dans les modèles à effet fixe séparés, lorsque comparé au placebo, le fébuxostat a réduit l'acide urique de 50% (P < 0,001), mais n'a eu aucun effet significatif sur les TBARS des tissus adipeux sous-cutanés (−7,4%, I.C. à 95% entre −57,4 et 101,4%), ni sur le niveau d'adiponectine (6,7%, I.C. à 95% entre −26,0% et 53,8%) ou sur le ratio TGF-ß/créatinine (18,0%, I.C. à 95% entre −10,0% et 54,8%). Il n'a pas non plus eu d'effets significatifs sur les critères secondaires. LIMITES DE L'ÉTUDE: La taille relativement modeste de l'échantillon, de même que la courte durée du suivi constituent les limites de l'étude. CONCLUSIONS: Dans la population observée, soit des patients atteints de néphropathie diabétique progressive, l'administration de fébuxostat a réduit de façon efficace les taux plasmatiques d'acide urique. Par ailleurs, aucun effet apparent n'a été observé sur les critères primaires et secondaires préétablis. ENREGISTREMENT DE L'ESSAI: Cette étude a été enregistrée sur clinicaltrials.gov (NCT01350388).
ABSTRACT
Hepatocyte growth factor (HGF) is a multifunctional cytokine that plays a crucial role in renal development, injury, and repair. HGF also serves a protective role in chronic renal disease by preventing tissue fibrosis. Endothelin-1 (ET-1), produced primarily by endothelial cells, is a potent vasoconstrictor that also acts as a proinflammatory peptide, promoting vascular injury and renal damage. In addition to mediating a variety of epithelial cell responses, HGF also induces hemodynamic changes that are poorly understood. The aim of the present study was to study the acute and chronic effects of HGF on ET-1 production in the kidney. We hypothesized that hemodynamic changes upon HGF treatment are likely mediated by immediate ET-1 release, whereas protection from renal fibrosis in rats chronically treated with HGF is likely due to suppression of ET-1 production. Acute HGF infusion into rats caused a decline in blood pressure that was enhanced by pretreatment with bosentan (an endothelin A and B receptor antagonist). HGF infusion also resulted in a decline in glomerular filtration rate (GFR) that could be entirely prevented by bosentan, suggesting that HGF acutely increases production and/or release of ET-1, which then mediates the observed decline in GFR. In cultured glomerular endothelial cells, HGF induced ET-1 production in a dose-dependent manner. Moreover, although there was an initial increase in ET-1 production upon HGF treatment, longer administration suppressed ET-1 production. This finding was consistent with the observation in vivo of a decrease in ET-1 production in renal parenchyma of rats chronically treated with HGF. Our data suggest both a hemodynamic and biological role for HGF-mediated ET-1 regulation.
