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Chronic kidney disease (CKD) has a high prevalence worldwide and is an intricate issue to whole medical society. Renal fibrosis is the common pathological feature for various kinds of CKD. As an anti‐aging protein, Klotho is predominantly expressed in renal tubular epithelial cells. Reports show Klotho could retard age‐related renal fibrosis. Mitochondrial dysfunction plays an important role in cellular senescence. However, the role of Klotho in mitochondrial dysfunction in CKD has not yet been determined. In this study, we treated unilateral ischemia‐reperfusion (UIRI) mice and cultured human renal tubular epithelial cells (HKC‐8) with Klotho. We assessed renal fibrosis, cellular senescence, and Wnt/β‐catenin signaling. We also focused on mitochondrial function assessment. In UIRI mice, ectopic expression of Klotho greatly retarded fibrotic lesions and the activation of Wnt/β‐catenin signaling. Interestingly, Klotho significantly preserved mitochondrial mass, inhibited mitochondrial reactive oxygen species (ROS) production and restored the expression of mitochondrial respiration chain complex subunits. Consequently, Klotho restrained cellular senescence. In HKC‐8 cells, Klotho significantly inhibited Wnt1‐ and Wnt9a‐induced mitochondrial injury, cellular senescence, and fibrotic lesions. These results suggest Klotho has a protective role in renal function through targeted protection on mitochondria. This further broads the understanding of the beneficial efficacies of Klotho in CKD. Our studies suggest Klotho has a protective role in renal function through targeted protection on mitochondria. This further broads the understanding of the beneficial efficacies of Klotho in CKD.

Micheliolide (MCL), derived from parthenolide (PTL), is known for its antioxidant and anti-inflammatory effects and has multiple roles in inflammatory diseases and tumours. To investigate its effect on renal disease, we intragastrically administrated DMAMCL, a dimethylamino Michael adduct of MCL for in vivo use, in two renal fibrosis models–the unilateral ureteral occlusion (UUO) model and an ischaemia-reperfusion injury (IRI) model and used MCL in combination with transforming growth factor beta 1 (TGF-β1) on mouse tubular epithelial cells (mTEC) in vitro. The expression of fibrotic markers (fibronectin and α-SMA) was remarkably reduced, while the expression of the epithelial marker E-cadherin was restored after DMAMCL treatment both in the UUO and IRI mice. MCL function in TGF-β1-induced epithelial-mesenchymal transition (EMT) in mTEC was consistent with the in vivo results. Metadherin (Mtdh) was activated in the fibrotic condition, suggesting that it might be involved in fibrogenesis. Interestingly, we found that while Mtdh was upregulated in the fibrotic condition, DMAMCL/MCL could suppress its expression. The overexpression of Mtdh exerted a pro-fibrotic effect by modulating the BMP/MAPK pathway in mTECs, and MCL could specifically reverse this effect. In conclusion, DMAMCL/MCL treatment represents a novel and effective therapy for renal fibrosis by suppressing the Mtdh/BMP/MAPK pathway.

Background Progressive peritoneal fibrosis is a worldwide public health concern impacting patients undergoing peritoneal dialysis (PD), yet there is no effective treatment. Our previous study revealed that a novel compound, micheliolide (MCL) inhibited peritoneal fibrosis in mice. However, its mechanism remains unclear. Brahma-related gene 1 (BRG1) is a key contributor to organ fibrosis, but its potential function in PD-related peritoneal fibrosis and the relationship between MCL and BRG1 remain unknown. Methods The effects of MCL on BRG1-induced fibrotic responses and TGF-β1-Smads pathway were examined in a mouse PD model and in vitro peritoneal mesothelial cells. To investigate the targeting mechanism of MCL on BRG1, coimmunoprecipitation, MCL-biotin pulldown, molecular docking and cellular thermal shift assay were performed. Results BRG1 was markedly elevated in a mouse PD model and in peritoneal mesothelial cells cultured in TGF-β1 or PD fluid condition. BRG1 overexpression in vitro augmented fibrotic responses and promoted TGF-β1-increased-phosphorylation of Smad2 and Smad3. Meanwhile, knockdown of BRG1 diminished TGF-β1-induced fibrotic responses and blocked TGF-β1-Smad2/3 pathway. MCL ameliorated BRG1 overexpression-induced peritoneal fibrosis and impeded TGF-β1-Smad2/3 signaling pathway both in a mouse PD model and in vitro. Mechanically, MCL impeded BRG1 from recognizing and attaching to histone H3 lysine 14 acetylation by binding to the asparagine (N1540) of BRG1, in thus restraining fibrotic responses and TGF-β1-Smad2/3 signaling pathway. After the mutation of N1540 to alanine (N1540A), MCL was unable to bind to BRG1 and thus, unsuccessful in suppressing BRG1-induced fibrotic responses and TGF-β1-Smad2/3 signaling pathway. Conclusion Our research indicates that BRG1 may be a crucial mediator in peritoneal fibrosis and MCL targeting N1540 residue of BRG1 may be a novel therapeutic strategy to combat PD-related peritoneal fibrosis.

Organic micro-pollutants such as pesticides and endocrine disruptors cause serious harm to human health and aquatic ecosystem. In this study, the potential degradation of atrazine (ATZ), triclosan (TCS), and 2,4,6-trichloroanisole (TCA) by UV-activated peroxydisulfate (UV/PDS) and UV-activated H 2 O 2 (UV/H 2 O 2 ) processes were evaluated under different conditions. Results showed that UV/PDS process was more effective than UV/H 2 O 2 under the same conditions. Increasing oxidant dosage or decreasing the initial ATZ, TCS, and TCA concentrations promoted the degradation rates of these three compounds. The presence of natural organic matter (NOM) could effectively scavenge sulfate radical (SO 4 • − ) and hydroxyl radical (HO•) and reduced the removal rates of target compounds. Degradation rates of ATZ and TCA decreased with pH increasing from 5.0 to 9.0 in UV/PDS process, while in UV/H 2 O 2 process, the increase of solution pH had little effect on ATZ and TCA degradation. In the UV/PDS and UV/H 2 O 2 oxidation process, when the solution pH increased from 5 to 8, the removal rates of TCS decreased by 19% and 1%, while when the solution pH increased to 9, the degradation rates of TCS increased by 23% and 17%. CO 3 2− /HCO 3 − had a small inhibitory effect on ATZ and TCA degradation by UV/H 2 O 2 and UV/PDS processes but promoted the degradation of TCS significantly (> 2 mM). Cl − had little effect on the degradation of ATZ, TCA, and TCS in UV/H 2 O 2 process. Cl − significant inhibited on the degradation of ATZ and TCS, but the influence of Cl − on the degradation of TCA was weak in UV/PDS process. Based on these experimental results, the various contributions of those secondary radicals (i.e., carbonate radical, chlorine radical) were discussed. This study can contribute to better understand the reactivities when UV/PDS and UV/H 2 O 2 are applied for the treatment of micro-pollutant-containing waters.

Chronic kidney disease is a common disease closely related to renal tubular inflammation and oxidative stress, and no effective treatment is available. Activation of the nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome is an important factor in renal inflammation, but the mechanism remains unclear. Micheliolide (MCL), which is derived from parthenolide, is a new compound with antioxidative and anti-inflammatory effects and has multiple roles in tumors and inflammatory diseases. In this study, we investigated the effect of MCL on lipopolysaccharide- (LPS-) induced inflammation in renal tubular cells and the related mechanism. We found that MCL significantly suppressed the LPS-induced NF-κB signaling and inflammatory expression of cytokines, such as tumor necrosis factor-α and monocyte chemoattractant protein-1 in a rat renal proximal tubular cell line (NRK-52E). MCL also prevented LPS- and adenosine triphosphate-induced NLRP3 inflammasome activation in vitro, as evidenced by the inhibition of NLRP3 expression, caspase-1 cleavage, and interleukin-1β and interleukin-18 maturation and secretion. Additionally, MCL inhibited the reduction of mitochondrial membrane potential and decreases the release of reactive oxygen species (ROS). Moreover, MCL can prevent NLRP3 inflammasome activation induced by rotenone, a well-known mitochondrial ROS (mROS) agonist, indicating that the mechanism of MCL’s anti-inflammatory effect may be closely related to the mROS. In conclusion, our study indicates that MCL can inhibit LPS-induced renal inflammation through suppressing the mROS/NF-κB/NLRP3 axis in tubular epithelial cells.

A novel, functionalized bubble surface can be obtained in dissolved air flotation （DAF） by dosing chemicals in the saturator. In this study, different cationic chemicals were used as bubble surface modifiers, and their effects on natural organic matter （NOM） removal from river water were investigated. NOM in the samples was fractionated based on molecular weight and hydrophobicity. The disinfection byproduct formation potentials of each fraction and their removal efficiencies were also evaluated. The results showed that chitosan was the most promising bubble modifier compared with a surfactant and a synthetic polymer. Tiny bubbles in the OAF pump system facilitated the adsorption of chitosan onto microbubble surfaces. The hydrophobic NOM fraction was preferentially removed by chitosan-modified bubbles. Decreasing the recycle water pH from 7.0 to 5.5 improved the removal of hydrophilic NOM with low molecular weight. Likewise, hydrophilic organic compounds gave high dihaloacetic acid yields in raw water. An enhanced reduction of haloacetic acid precursors was obtained with recycle water at pH values of 5.5 and 4.0. The experimental results indicate that NOM fractions may interact with bubbles through different mechanisms. Positive bubble modification provides an alternative approach for OAF to enhance NOM removal.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Renal fibrosis is the common pathological feature in a variety of chronic kidney diseases. Aging is highly associated with the progression of renal fibrosis. Among several determinants, mitochondrial dysfunction plays an important role in aging. However, the underlying mechanisms of mitochondrial dysfunction in age‐related renal fibrosis are not elucidated. Herein, we found that Wnt/β‐catenin signaling and renin–angiotensin system (RAS) activity were upregulated in aging kidneys. Concomitantly, mitochondrial mass and functions were impaired with aging. Ectopic expression of Klotho, an antagonist of endogenous Wnt/β‐catenin activity, abolished renal fibrosis in d‐galactose (d‐gal)‐induced accelerated aging mouse model and significantly protected renal mitochondrial functions by preserving mass and diminishing the production of reactive oxygen species. In an established aging mouse model, dickkopf 1, a more specific Wnt inhibitor, and the mitochondria‐targeted antioxidant mitoquinone restored mitochondrial mass and attenuated tubular senescence and renal fibrosis. In a human proximal tubular cell line (HKC‐8), ectopic expression of Wnt1 decreased biogenesis and induced dysfunction of mitochondria, and triggered cellular senescence. Moreover, d‐gal triggered the transduction of Wnt/β‐catenin signaling, which further activated angiotensin type 1 receptor (AT1), and then decreased the mitochondrial mass and increased cellular senescence in HKC‐8 cells and primary cultured renal tubular cells. These effects were inhibited by AT1 blocker of losartan. These results suggest inhibition of Wnt/β‐catenin signaling and the RAS could slow the onset of age‐related mitochondrial dysfunction and renal fibrosis. Taken together, our results indicate that Wnt/β‐catenin/RAS signaling mediates age‐related renal fibrosis and is associated with mitochondrial dysfunction. Wnt/β‐catenin signaling induces RAS activation, which promotes cellular senescence and age‐related kidney fibrosis in association with mitochondrial dysfunction that stems from a loss of mitochondrial biogenesis.

In this study, an N-ZnO/g-C 3 N 4 (g-N-Z) Z-scheme photocatalyst was constructed using hydrothermal and high-temperature calcination. X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FT-IR), X-ray photoelectron spectroscopy (XPS), and other tests were employed to characterise the catalytic material. The results showed that after N-ZnO modification, the separation efficiency of the photoinduced charge pairs and the utilisation of sunlight in the composites were improved. The kinetics experiments indicated that the degradation of atrazine (ATZ) in the g-N-Z/PDS/solar system was significantly better than that in the PDS/solar system. Under the action of the g-N-Z/PDS/solar system, the degradation rate of ATZ reached 83.88%, whereas in the PDS/solar system, it was only 31.76%. In addition, it was found that increasing the PDS concentration, g-N-Z dosage, and solution acidity effectively accelerated the removal of ATZ. The presence of HCO 3 − /CO 3 2− , Cl − , and natural organic matter (NOM) inhibited the oxidation efficiency of the g-N-Z/PDS/solar system. Moreover, the presence of multiple reactive oxygen species (ROS) was confirmed using radical scavenging experiments to determine the contribution of each active component. Twelve oxidation intermediates of ATZ were obtained via liquid chromatography-tandem mass spectrometry (LC–MS/MS), and the mechanism of enhanced ATZ degradation in the g-N-Z/PDS/solar system was proposed. Actual water and cyclic photocatalytic experiments further suggest that g-N-Z has good application value in water treatment.

Selective adsorption of Pb(II) and Cr(VI) by surfactant-modified and unmodified zeolites is discussed in this paper. The influences of pH, ionic strength, temperature, and adsorption time on Cr(VI) and Pb(II) adsorption are studied, The characteristics of the surface and inner structures of zeolites before and after modification are analyzed through infrared spectroscopy, scanning electron microscopy, X-ray diffraction, Brunauer–Emmett–Teller analysis, and zeta potential measurement. Results show that the characteristics of electric charge on the zeolite surface had changed after modification, which resulted in selective adsorption of Cr(VI) and Pb(II). Moreover, kinetic study reveals that adsorption by the different zeolites coincides with the Langmuir model and pseudo-second-order kinetic equation. The intraparticle diffusion equation proves that the Cr(VI) adsorption is mainly electrostatic, whereas Pb(II) adsorption proceeds via intrapore and electrostatic adsorption on the zeolite surface. This difference in mechanisms endows selectivity of metal ion adsorption by the modified zeolites. This study provides a reference on zeolite modification for use in various applications, such as wastewater treatment.