scholarly journals Reactive oxygen species and acute kidney injury after trauma in obese rats (859.2)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Peter Mittwede ◽  
Lusha Xiang ◽  
Silu Lu ◽  
John Clemmer ◽  
Robert Hester
Keyword(s):  
Reactive Oxygen Species ◽  
Acute Kidney Injury ◽  
Reactive Oxygen ◽  
Kidney Injury ◽  
Oxygen Species ◽  
Obese Rats

scholarly journals Exogenous pentraxin-3 inhibits the reactive oxygen species-mitochondrial and apoptosis pathway in acute kidney injury

PLoS ONE ◽  
2018 ◽  
Vol 13 (4) ◽  
pp. e0195758 ◽  
Author(s):  
Hyung Ho Lee ◽  
Sook Young Kim ◽  
Joon Chae Na ◽  
Young Eun Yoon ◽  
Woong Kyu Han
Keyword(s):  
Reactive Oxygen Species ◽  
Acute Kidney Injury ◽  
Reactive Oxygen ◽  
Kidney Injury ◽  
Oxygen Species ◽  
Pentraxin 3 ◽  
Apoptosis Pathway

scholarly journals Treatment of Acute Kidney Injury Using a Dual Enzyme Embedded Zeolitic Imidazolate Frameworks Cascade That Catalyzes In Vivo Reactive Oxygen Species Scavenging

2022 ◽  
Vol 9 ◽  
Author(s):  
Xinyue Hou ◽  
Jianxiang Shi ◽  
Jie Zhang ◽  
Zhigang Wang ◽  
Sen Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Acute Kidney Injury ◽  
Effective Means ◽  
Antioxidant Properties ◽  
Reactive Oxygen ◽  
Kidney Injury ◽  
Oxygen Species ◽  
Zeolitic Imidazolate Frameworks ◽  
Zeolitic Imidazolate Framework ◽  
Intracellular Enzyme

Significant advances have been made in recent years for the utilization of natural enzymes with antioxidant properties to treat acute kidney injury (AKI). However, these enzymes have been of limited clinical utility because of their limited cellular uptake, poor pharmacokinetic properties, and suboptimal stability. We employed a novel biomimetic mineralization approach to encapsulate catalase (CAT) and superoxide dismutase (SOD) in a zeolitic imidazolate framework-8 (ZIF-8). Next, this SOD@CAT@ZIF-8 complex was anchored with MPEG2000-COOH to yield an MPEG2000-SOD@CAT@ZIF-8 (PSCZ) composite. The composite was then used as a stable tool with antioxidant properties for the integrated cascade-based treatment of AKI, remarkably improved intracellular enzyme delivery. This dual-enzyme-embedded metal-organic framework could effectively scavenge reactive oxygen species. In conclusion, the ZIF-8-based “armor plating” represents an effective means of shielding enzymes with improved therapeutic utility to guide the precision medicine-based treatment of AKI.

scholarly journals BAM15 treats mouse sepsis and sepsis-AKI, linking circulating mitochondrial DNA and tubule reactive oxygen species

2021 ◽  
Author(s):  
Naoko Tsuji ◽  
Takayuki Tsuji ◽  
Tetsushi Yamashita ◽  
Xuzhen Hu ◽  
Peter S.T. Yuen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mitochondrial Dna ◽  
Precision Medicine ◽  
Cecal Ligation ◽  
Reactive Oxygen ◽  
Kidney Injury ◽  
Experimental Sepsis ◽  
Oxygen Species ◽  
Clinical Sepsis

The pathogenesis of sepsis is complex and heterogeneous; hence, a precision medicine strategy may be required. Acute kidney injury (AKI) following sepsis portends higher mortality. Overproduction of mitochondrial reactive oxygen species (mtROS) is a potential mediator of sepsis and sepsis-induced AKI. BAM15 is a chemical uncoupler that dissipates the mitochondrial proton gradient without generating mtROS, and improves experimental renal ischemic injury. We injected BAM15 into mice at 0 or 6 hours after cecal ligation and puncture (CLP) treated with fluids and antibiotics. BAM15 reduced mortality, even when started at 6 hours, when mice were ill, and reduced kidney damage but did not affect other organs. Serial plasma and urinary levels of mitochondrial DNA (mtDNA) were increased following CLP, and decreased after BAM15 (at 0 and at 6 hours). In vitro BAM15 prevented mtROS overproduction and mtDNA release from septic kidney tubule cells; mtROS generation correlated with mtDNA release. BAM15 also promotes mitochondrial biogenesis signaling. We conclude that BAM15 is an effective preventive and therapeutic candidate in experimental sepsis, and that BAM15 and mtDNA are mechanistically linked via mtROS, which may form a drug-companion diagnostic pair to improve precision medicine approaches to diagnosing and treating clinical sepsis.

scholarly journals Intracellular Reactive Oxygen Species Mediate the Therapeutic Effect of Induced Pluripotent Stem Cells for Acute Kidney Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Shun Wang ◽  
Xiaoyu Tian ◽  
Yijun Li ◽  
Rong Xue ◽  
Haochen Guan ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Acute Kidney Injury ◽  
Therapeutic Effect ◽  
Pluripotent Stem Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Oxygen Species ◽  
Renal Ischemia Reperfusion Injury ◽  
Induced Pluripotent

Aims. Treatment for acute kidney injury (AKI) is challenging. Induced pluripotent stem cells (iPSCs) have great therapeutic potential. This study sought to determine whether iPSCs attenuate AKI and the role of reactive oxygen species (ROS). Results. We intravenously injected isogenic iPSCs into mice 2 h after renal ischemia-reperfusion injury (IRI). The cells were selectively trafficked to ischemia/reperfusion-injured kidney where they decreased kidney ROS and inflammatory cytokines and improved kidney function and morphology. Pretreating the cells with ROS inhibitors before administration decreased iPSC engraftment and abolished the protective effect of iPSCs. In contrast, pretreating iPSCs with hydrogen peroxide increased iPSC engraftment and therapeutic effect. Although the intravenously administered iPSCs trafficked to the IRI kidney, the cells did not differentiate into proximal or distal tubular epithelial cells. In vitro, the capabilities of the iPSC-released substances to promote proliferation and decrease apoptosis of renal epithelial cells were increased by ROS pretreatment of iPSCs. Moreover, pretreatment of the iPSCs with ROS inhibitor had the opposite effect. Similarly, moderate concentrations of ROS increased while ROS inhibitors decreased iPSC mobility, adhesion to the extracellular matrix, and mitochondrial metabolism. Innovation and Conclusion. iPSCs decreased renal ischemia/reperfusion injury mainly through iPSC-released substances. The therapeutic effect, mitochondrial metabolism, mobility, and kidney trafficking of iPSCs were ROS dependent.

scholarly journals Pericardial Adipose Tissue–Derived Leptin Promotes Myocardial Apoptosis in High‐Fat Diet–Induced Obese Rats Through Janus Kinase 2/Reactive Oxygen Species/Na+/K+‐ATPase Signaling Pathway

2021 ◽  
Author(s):  
Ping Wang ◽  
Chaodi Luo ◽  
Danjun Zhu ◽  
Yan Song ◽  
Lifei Cao ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Adipose Tissue ◽  
High Fat Diet ◽  
Reactive Oxygen ◽  
Janus Kinase ◽  
Oxygen Species ◽  
High Fat ◽  
Myocardial Apoptosis ◽  
Pericardial Adipose Tissue ◽  
Obese Rats

Background Pathophysiologic mechanisms underlying cardiac structural and functional changes in obesity are complex and linked to adipocytokines released from pericardial adipose tissue (PAT) and cardiomyocyte apoptosis. Although leptin is involved in various pathological conditions, its role in paracrine action of pericardial adipose tissue on myocardial apoptosis remains unknown. This study was designed to investigate the role of PAT‐derived leptin on myocardial apoptosis in high‐fat diet–induced obese rats. Methods and Results Hearts were isolated from lean or high‐fat diet–induced obese Wistar rats for myocardial remodeling studies. Obese rats had abnormal myocardial structure, diastolic dysfunction, greatly elevated cardiac apoptosis, enhanced cardiac fibrosis, and increased oxidative stress level. ELISA detected significantly higher than circulating leptin level in PAT of obese, but not lean, rats. Western blot and immunohistochemical analyses demonstrated increased leptin receptor density in obese hearts. H9c2 cardiomyoblasts, after being exposed to PAT‐conditioned medium of obese rats, exhibited pronounced reactive oxygen species–mediated apoptosis, which was partially reversed by leptin antagonist. Moreover, leptin derived from PAT of obese rats inhibited Na + /K + ‐ATPase activity of H9c2 cells through stimulating reactive oxygen species, thereby activating calcium‐dependent apoptosis. Pretreatment with specific inhibitors revealed that Janus kinase 2/signal transducer and activator of transcription 3 and phosphoinositide 3‐kinase/protein kinase B signaling pathways were involved in leptin‐induced myocardial apoptosis. Conclusions PAT‐derived leptin induces myocardial apoptosis in high‐fat diet–induced obese rats via activating Janus kinase 2/signal transducer and activator of transcription 3/reactive oxygen species signaling pathway and inhibiting its downstream Na + /K + ‐ATPase activity.

scholarly journals Different effects of global osteopontin and macrophage osteopontin in glomerular injury

2018 ◽  
Vol 315 (4) ◽  
pp. F759-F768 ◽  
Author(s):  
Jessica Trostel ◽  
Luan D. Truong ◽  
Carlos Roncal-Jimenez ◽  
Makoto Miyazaki ◽  
Shinobu Miyazaki-Anzai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Kidney Injury ◽  
Oxygen Species ◽  
Glomerular Injury ◽  
Tubulointerstitial Injury ◽  
Crescent Formation ◽  
Elevated Expression ◽  
Toxin Receptor

Osteopontin (OPN) is a pro-and anti-inflammatory molecule that simultaneously attenuates oxidative stress. Both inflammation and oxidative stress play a role in the pathogenesis of glomerulonephritis and in the progression of kidney injury. Importantly, OPN is highly induced in nephritic kidneys. To characterize further the role of OPN in kidney injury we used OPN−/− mice in antiglomerular basement membrane reactive serum-induced immune (NTS) nephritis, an inflammatory and progressive model of kidney disease. Normal wild-type (WT) and OPN−/− mice did not show histological differences. However, nephritic kidneys from OPN−/− mice showed severe damage compared with WT mice. Glomerular proliferation, necrotizing lesions, crescent formation, and tubulointerstitial injury were significantly higher in OPN−/− mice. Macrophage infiltration was increased in the glomeruli and interstitium in OPN−/− mice, with higher expression of IL-6, CCL2, and chemokine CXCL1. In addition, collagen (Col) I, Col III, and Col IV deposition were increased in kidneys from OPN−/− mice. Elevated expression of the reactive oxygen species-generating enzyme Nox4 and blunted expression of Nrf2, a molecule that inhibits reactive oxygen species and inflammatory pathways, was observed in nephritic kidneys from OPN−/− mice. Notably, CD11b diphteria toxin receptor mice with NTS nephritis selectively depleted of macrophages and reconstituted with OPN−/− macrophages showed less kidney injury compared with mice receiving WT macrophages. These findings suggest that in global OPN−/− mice there is increased inflammation and redox imbalance that mediate kidney damage. However, absence of macrophage OPN is protective, indicating that macrophage OPN plays a role in the induction and progression of kidney injury in NTS nephritis.

scholarly journals Why Is Diabetes Mellitus a Risk Factor for Contrast-Induced Nephropathy?

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Samuel N. Heyman ◽  
Christian Rosenberger ◽  
Seymour Rosen ◽  
Mogher Khamaisi
Keyword(s):  
Reactive Oxygen Species ◽  
Contrast Media ◽  
A Priori ◽  
Reactive Oxygen ◽  
Kidney Injury ◽  
Oxygen Species ◽  
Contrast Induced Nephropathy ◽  
Predisposing Factor ◽  
And Oxidative Stress ◽  
Regulation Of Vascular Tone

Contrast-induced nephropathy (CIN) remains a leading cause of iatrogenic acute kidney injury, as the usage of contrast media for imaging and intravascular intervention keeps expanding. Diabetes is an important predisposing factor for CIN, particularly in patients with renal functional impairment. Renal hypoxia, combined with the generation of reactive oxygen species, plays a central role in the pathogenesis of CIN, and the diabetic kidney is particularly susceptible to intensified hypoxic and oxidative stress following the administration of contrast media. The pathophysiology of this vulnerability is complex and involves various mechanisms, including a priori enhanced tubular transport activity, oxygen consumption, and the generation of reactive oxygen species. The regulation of vascular tone and peritubular blood flow may also be altered, particularly due to defective nitrovasodilation, enhanced endothelin production, and a particular hyperresponsiveness to adenosine-related vasoconstriction. In addition, micro- and macrovascular diseases and chronic tubulointerstitial changes further compromise regional oxygen delivery, and renal antioxidant capacity might be hampered. A better understanding of these mechanisms and their control in the diabetic patient may initiate novel strategies in the prevention of contrast nephropathy in these susceptible patients.

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