Zeolite Composite Nanofiber Mesh for Indoxyl Sulfate Adsorption toward Wearable Blood Purification Devices

A nanofiber mesh was prepared for the adsorption of indoxyl sulfate (IS), a toxin associated with chronic kidney disease. Removing IS is highly demanded for efficient blood purification. The objective of this study is to develop a zeolite composite nanofiber mesh to remove IS efficiently. Eight zeolites with different properties were used for IS adsorption, where a zeolite with a pore size of 7 Å, H+ cations, and a silica to aluminum ratio of 240 mol/mol exhibited the highest adsorption capacity. This was primarily attributed to its suitable silica to aluminum ratio. The zeolites were incorporated in biocompatible poly (ethylene-co-vinyl alcohol) (EVOH) nanofibers, and a zeolite composite nanofiber mesh was successfully fabricated via electrospinning. The nanofiber mesh exhibited an IS adsorption capacity of 107 μg/g, while the adsorption capacity by zeolite increased from 208 μg/g in powder form to 386 μg/g when dispersed in the mesh. This also led to an increase in cell viability from 86% to 96%. These results demonstrated that this zeolite composite nanofiber mesh can be safely and effectively applied in wearable blood purification devices.

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Highly porous starch/poly(ethylene-alt -maleic anhydride) composite nanofiber mesh

Polymer Composites ◽

10.1002/pc.22545 ◽

2013 ◽

Vol 34 (8) ◽

pp. 1321-1324 ◽

Cited By ~ 19

Author(s):

Burcu Oktay ◽

Emre Baştürk ◽

Nilhan Kayaman-Apohan ◽

Memet Vezir Kahraman

Keyword(s):

Maleic Anhydride ◽

Composite Nanofiber ◽

Poly Ethylene ◽

Highly Porous ◽

Nanofiber Mesh

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Uremic toxin indoxyl sulfate promotes proinflammatory macrophage activation by regulation of β-catenin and YAP pathways

Journal of Molecular Histology ◽

10.1007/s10735-020-09936-y ◽

2021 ◽

Author(s):

Ying Li ◽

Jing Yan ◽

Minjia Wang ◽

Jing Lv ◽

Fei Yan ◽

...

Keyword(s):

Cardiovascular Disease ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Inflammatory Response ◽

Macrophage Polarization ◽

Indoxyl Sulfate ◽

Uremic Toxin ◽

Lps Challenge ◽

Hla Dr ◽

M1 Macrophage

AbstractEvidence has been shown that indoxyl sulfate (IS) could impair kidney and cardiac functions. Moreover, macrophage polarization played important roles in chronic kidney disease and cardiovascular disease. IS acts as a nephron-vascular toxin, whereas its effect on macrophage polarization during inflammation is still not fully elucidated. In this study, we aimed to investigate the effect of IS on macrophage polarization during lipopolysaccharide (LPS) challenge. THP-1 monocytes were incubated with phorbol 12-myristate-13-acetate (PMA) to differentiate into macrophages, and then incubated with LPS and IS for 24 h. ELISA was used to detect the levels of TNFα, IL-6, IL-1β in THP-1-derived macrophages. Western blot assay was used to detect the levels of arginase1 and iNOS in THP-1-derived macrophages. Percentages of HLA-DR-positive cells (M1 macrophages) and CD206-positive cells (M2 macrophages) were detected by flow cytometry. IS markedly increased the production of the pro-inflammatory factors TNFα, IL-6, IL-1β in LPS-stimulated THP-1-derived macrophages. In addition, IS induced M1 macrophage polarization in response to LPS, as evidenced by the increased expression of iNOS and the increased proportion of HLA-DR+ macrophages. Moreover, IS downregulated the level of β-catenin, and upregulated the level of YAP in LPS-stimulated macrophages. Activating β-catenin signaling or inhibiting YAP signaling suppressed the IS-induced inflammatory response in LPS-stimulated macrophages by inhibiting M1 polarization. IS induced M1 macrophage polarization in LPS-stimulated macrophages via inhibiting β-catenin and activating YAP signaling. In addition, this study provided evidences that activation of β-catenin or inhibition of YAP could alleviate IS-induced inflammatory response in LPS-stimulated macrophages. This finding may contribute to the understanding of immune dysfunction observed in chronic kidney disease and cardiovascular disease.

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Morphological, Thermal, and Mechanical Properties of Electrospun Recycled Poly(ethylene terephthalate)/Graphene Oxide Composite Nanofiber Membranes

ACS Omega ◽

10.1021/acsomega.1c02578 ◽

2021 ◽

Author(s):

Koena Selatile ◽

Suprakas Sinha Ray ◽

Vincent Ojijo ◽

Rotimi Emmanuel Sadiku

Keyword(s):

Mechanical Properties ◽

Graphene Oxide ◽

Ethylene Terephthalate ◽

Thermal And Mechanical Properties ◽

Oxide Composite ◽

Poly Ethylene Terephthalate ◽

Composite Nanofiber ◽

Nanofiber Membranes ◽

Poly Ethylene

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Indoxyl-Sulfate-Induced Redox Imbalance in Chronic Kidney Disease

Antioxidants ◽

10.3390/antiox10060936 ◽

2021 ◽

Vol 10 (6) ◽

pp. 936

Author(s):

Chien-Lin Lu ◽

Cai-Mei Zheng ◽

Kuo-Cheng Lu ◽

Min-Tser Liao ◽

Kun-Lin Wu ◽

...

Keyword(s):

Oxidative Stress ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Muscle Wasting ◽

Mesangial Cells ◽

Target Organ Damage ◽

Organ Damage ◽

Indoxyl Sulfate ◽

Uremic Toxin ◽

Tubulointerstitial Injury

The accumulation of the uremic toxin indoxyl sulfate (IS) induces target organ damage in chronic kidney disease (CKD) patients, and causes complications including cardiovascular diseases, renal osteodystrophy, muscle wasting, and anemia. IS stimulates reactive oxygen species (ROS) production in CKD, which impairs glomerular filtration by a direct cytotoxic effect on the mesangial cells. IS further reduces antioxidant capacity in renal proximal tubular cells and contributes to tubulointerstitial injury. IS-induced ROS formation triggers the switching of vascular smooth muscular cells to the osteoblastic phenotype, which induces cardiovascular risk. Low-turnover bone disease seen in early CKD relies on the inhibitory effects of IS on osteoblast viability and differentiation, and osteoblastic signaling via the parathyroid hormone. Excessive ROS and inflammatory cytokine releases caused by IS directly inhibit myocyte growth in muscle wasting via myokines’ effects. Moreover, IS triggers eryptosis via ROS-mediated oxidative stress, and elevates hepcidin levels in order to prevent iron flux in circulation in renal anemia. Thus, IS-induced oxidative stress underlies the mechanisms in CKD-related complications. This review summarizes the underlying mechanisms of how IS mediates oxidative stress in the pathogenesis of CKD’s complications. Furthermore, we also discuss the potential role of oral AST-120 in attenuating IS-mediated oxidative stress after gastrointestinal adsorption of the IS precursor indole.

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Synbiotics Alleviate the Gut Indole Load and Dysbiosis in Chronic Kidney Disease

Cells ◽

10.3390/cells10010114 ◽

2021 ◽

Vol 10 (1) ◽

pp. 114

Author(s):

Chih-Yu Yang ◽

Ting-Wen Chen ◽

Wan-Lun Lu ◽

Shih-Shin Liang ◽

Hsien-Da Huang ◽

...

Keyword(s):

Chronic Kidney Disease ◽

Kidney Disease ◽

Gut Microbiota ◽

Statistical Significance ◽

Additional Treatment ◽

Indoxyl Sulfate ◽

Uremic Toxin ◽

Healthy Controls ◽

Gut Dysbiosis ◽

Novel Concept

Chronic kidney disease (CKD) has long been known to cause significant digestive tract pathology. Of note, indoxyl sulfate is a gut microbe-derived uremic toxin that accumulates in CKD patients. Nevertheless, the relationship between gut microbiota, fecal indole content, and blood indoxyl sulfate level remains unknown. In our study, we established an adenine-induced CKD rat model, which recapitulates human CKD-related gut dysbiosis. Synbiotic treatment in CKD rats showed a significant reduction in both the indole-producing bacterium Clostridium and fecal indole amount. Furthermore, gut microbiota diversity was reduced in CKD rats but was restored after synbiotic treatment. Intriguingly, in our end-stage kidney disease (ESKD) patients, the abundance of indole-producing bacteria, Bacteroides, Prevotella, and Clostridium, is similar to that of healthy controls. Consistently, the fecal indole tends to be higher in the ESKD patients, but the difference did not achieve statistical significance. However, the blood level of indoxyl sulfate was significantly higher than that of healthy controls, implicating that under an equivalent indole production rate, the impaired renal excretion contributes to the accumulation of this notorious uremic toxin. On the other hand, we did identify two short-chain fatty acid-producing bacteria, Faecalibacterium and Roseburia, were reduced in ESKD patients as compared to the healthy controls. This may contribute to gut dysbiosis. We also identified that three genera Fusobacterium, Shewanella, and Erwinia, in the ESKD patients but not in the healthy controls. Building up gut symbiosis to treat CKD is a novel concept, but once proved effective, it will provide an additional treatment strategy for CKD patients.

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