scholarly journals Cytotoxicity and oxidative stress induced by different metallic nanoparticles on human kidney cells

2011 ◽  
Vol 8 (1) ◽  
pp. 10 ◽  
Author(s):  
Igor Pujalté ◽  
Isabelle Passagne ◽  
Brigitte Brouillaud ◽  
Mona Tréguer ◽  
Etienne Durand ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metallic Nanoparticles ◽  
Human Kidney ◽  
Kidney Cells ◽  
And Oxidative Stress

Study of different metallic nanoparticles on human kidney cells: Toxicity and oxidative stress

2011 ◽  
Vol 205 ◽  
pp. S172
Author(s):  
I. Pujalté ◽  
I. Passagne ◽  
B. Brouillaud ◽  
R. Daculsi ◽  
M. Tréguer ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metallic Nanoparticles ◽  
Human Kidney ◽  
Kidney Cells ◽  
And Oxidative Stress

scholarly journals Cudrania tricuspidata Root Extract Prevents Methylglyoxal-Induced Inflammation and Oxidative Stress via Regulation of the PKC-NOX4 Pathway in Human Kidney Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Donghee Kim ◽  
Jayeon Cheon ◽  
Haelim Yoon ◽  
Hee-Sook Jun
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase ◽  
Antioxidant Enzyme ◽  
Root Extract ◽  
Kidney Cells ◽  
Nuclear Factor ◽  
Ros Production ◽  
Cudrania Tricuspidata ◽  
Pkc Activation ◽  
And Oxidative Stress

Diabetic nephropathy is a microvascular complication induced by diabetes, and methylglyoxal (MGO) is a reactive carbonyl species causing oxidative stress that contributes to the induction of inflammatory response in kidney cells. Cudrania tricuspidata (CT), cultivated in Northeast Asia, has been used as traditional medicine for treating various diseases, including neuritis, liver damage, and cancer. In this study, we determined whether a CT root extract (CTRE) can prevent MGO-induced reactive oxygen species (ROS) production and inflammation and assessed underlying mechanisms using a kidney epithelial cell line, HK-2. We observed that CTRE inhibited MGO-induced ROS production. Additionally, CTRE ameliorated the activation of MGO-induced inflammatory signaling pathways such as p38 mitogen-activated protein kinase (MAPK), extracellular signal-regulated kinase (ERK), and c-JUN N-terminal kinase (JNK). Consistent with these results, expressions of p-nuclear factor-kappa B (NFκB) and inflammatory cytokines, tumor necrosis factor-α, interleukin- (IL-) 1β, and IL-6, were decreased when compared with MGO-only exposed HK-2 cells. CTRE alleviated the MGO-induced decrease in nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and antioxidant enzyme mRNA expressions. MGO induced the expression of NADPH oxidase 4 (NOX4); CTRE pretreatment inhibited this induction. Further studies revealed that the NOX4 expression was inhibited owing to the suppression of MGO-induced protein kinase C (PKC) activation following CTRE treatment. Collectively, our data suggest that CTRE attenuates MGO-induced inflammation and oxidative stress via inhibition of PKC activation and NOX4 expression, as well as upregulating the Nrf2-antioxidant enzyme pathway in HK-2 cells.

scholarly journals microRNA-200c regulates KLOTHO expression in human kidney cells under oxidative stress

PLoS ONE ◽  
2019 ◽  
Vol 14 (6) ◽  
pp. e0218468 ◽  
Author(s):  
Kenichi Morii ◽  
Satoshi Yamasaki ◽  
Shigehiro Doi ◽  
Taisuke Irifuku ◽  
Kensuke Sasaki ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Human Kidney ◽  
Kidney Cells

scholarly journals Kidney Organoids as a Novel Platform to Evaluate Lipopolysaccharide-Induced Oxidative Stress and Apoptosis in Acute Kidney Injury

2021 ◽  
Vol 8 ◽  
Author(s):  
Weitao Zhang ◽  
Ruochen Qi ◽  
Tingting Li ◽  
Xuepeng Zhang ◽  
Yi Shi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Immune Cell ◽  
Kidney Injury ◽  
Human Kidney ◽  
Kidney Cells ◽  
Pathological Changes ◽  
Kidney Organoids

Sepsis-associated acute kidney injury (SA-AKI) is a life-threatening syndrome. Lipopolysaccharide (LPS) is a widely used inducer for modeling SA-AKI both in vivo and in vitro. However, due to the innate complexity of the kidney architecture, the mechanisms underlying the pathogenesis of SA-AKI, as well as those involved in LPS-induced kidney injury remain to be clarified. Kidney organoids derived from human pluripotent stem cells (hPSCs) act as a model of multiple types of kidney cells in vitro and eliminate potential confounders in vivo. In the current study, we established LPS-induced kidney injury models both in vivo and in human kidney organoids. Kidney function, pathological changes, and markers of oxidative stress were evaluated with/without the presence of methylprednisolone (MP) treatment both in vivo and in vitro. The extent of LPS-induced oxidative stress and apoptosis in kidney organoids was further investigated in vitro. LPS-induced acute kidney injury in mice, together with pathological changes and increased oxidative stress, as well as enhanced apoptosis in kidney cells were evaluated. These phenomena were ameliorated by MP treatment. Experiments in kidney organoids showed that the LPS-induced apoptotic effects occurred mainly in podocytes and proximal tubular cells. Our experiments demonstrated the efficacy of using kidney organoids as a solid platform to study LPS-induced kidney injury. LPS induced oxidative stress as well as apoptosis in kidney cells independently of changes in perfusion or immune cell infiltration. MP treatment partially alleviated LPS-induced injury by reducing kidney cell oxidative stress and apoptosis.

scholarly journals Diphlorethohydroxycarmalol Attenuates Methylglyoxal-Induced Oxidative Stress and Advanced Glycation End Product Formation in Human Kidney Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-14 ◽  
Author(s):  
Seon-Heui Cha ◽  
Yongha Hwang ◽  
Soo-Jin Heo ◽  
Hee-Sook Jun
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Mrna Expression ◽  
Human Kidney ◽  
Product Formation ◽  
Diabetic Patients ◽  
Kidney Cells ◽  
Advanced Glycation ◽  
Advanced Glycation End Product ◽  
Hek Cells

Diabetic nephropathy is the leading cause of end-stage renal disease in patients with diabetes mellitus. Oxidative stress has been shown to play an important role in pathogeneses of renal damage in diabetic patients. Here, we investigated the protective effect of diphlorethohydroxycarmalol (DPHC), which is a polyphenol isolated from an edible seaweed, Ishige okamurae, on methylglyoxal-induced oxidative stress in HEK cells, a human embryonic kidney cell line. DPHC treatment inhibited methylglyoxal- (MGO-) induced cytotoxicity and ROS production. DPHC activated the Nrf2 transcription factor and increased the mRNA expression of antioxidant and detoxification enzymes, consequently reducing MGO-induced advanced glycation end product formation. In addition, DPHC increased glyoxalase-1 mRNA expression and attenuated MGO-induced advanced glycation end product formation in HEK cells. These results suggest that DPHC possesses a protective activity against MGO-induced cytotoxicity in human kidney cells by preventing oxidative stress and advanced glycation end product formation. Therefore, it could be used as a potential therapeutic agent for the prevention of diabetic nephropathy.

1107: Evaluation of Cystine Transport in Cultured Human Kidney Cells: Primer to Gene Therapy of Cystinuria

2005 ◽  
Vol 173 (4S) ◽  
pp. 300-300
Author(s):  
Sreedhar Sagi ◽  
Lutz Trojan ◽  
Peter Aiken ◽  
Maurice S. Michel ◽  
Thomas Knoll
Keyword(s):  
Gene Therapy ◽  
Human Kidney ◽  
Kidney Cells

Association between calcitriol and paricalcitol with oxidative stress in patients with hemodialysis

2020 ◽  
pp. 1-8
Author(s):  
Hasan Haci Yeter ◽  
Berfu Korucu ◽  
Elif Burcu Bali ◽  
Ulver Derici
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Antioxidant Status ◽  
Total Antioxidant Status ◽  
Stress Index ◽  
Total Oxidant Status ◽  
Vitamin D Analog ◽  
Total Antioxidant ◽  
Oxidant Status ◽  
And Oxidative Stress

Abstract. Background: The pathophysiological basis of chronic kidney disease and its complications, including cardiovascular disease, are associated with chronic inflammation and oxidative stress. We investigated the effects of active vitamin D (calcitriol) and synthetic vitamin D analog (paricalcitol) on oxidative stress in hemodialysis patients. Methods: This cross-sectional study was composed of 83 patients with a minimum hemodialysis vintage of one year. Patients with a history of any infection, malignancy, and chronic inflammatory disease were excluded. Oxidative markers (total oxidant and antioxidant status) and inflammation markers (C-reactive protein and interleukin-6) were analyzed. Results: A total of 47% (39/83) patients were using active or analog vitamin D. Total antioxidant status was significantly higher in patients with using active or analog vitamin D than those who did not use (p = 0.006). Whereas, total oxidant status and oxidative stress index were significantly higher in patients with not using vitamin D when compared with the patients who were using vitamin D preparation (p = 0.005 and p = 0.004, respectively). On the other hand, total antioxidant status, total oxidant status, and oxidative stress index were similar between patients who used active vitamin D or vitamin D analog (p = 0.6; p = 0.4 and p = 0.7, respectively). Conclusion: The use of active or selective vitamin D analog in these patients decreases total oxidant status and increases total antioxidant status. Also, paricalcitol is as effective as calcitriol in decreasing total oxidant status and increasing total antioxidant status in patients with chronic kidney disease.

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