scholarly journals Nox4 has a crucial role in uric acid-induced oxidative stress and apoptosis in renal tubular cells

2016 ◽  
Vol 13 (5) ◽  
pp. 4343-4348 ◽  
Author(s):  
Zhuohang Li ◽  
Yiyu Sheng ◽  
Cheng Liu ◽  
Kuiqing Li ◽  
Xin Huang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Crucial Role ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

scholarly journals Telmisartan Attenuates Uric Acid-Induced Epithelial-Mesenchymal Transition in Renal Tubular Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Dongqing Zha ◽  
Saiqun Wu ◽  
Ping Gao ◽  
Xiaoyan Wu
Keyword(s):  
Uric Acid ◽  
Epithelial Cells ◽  
Nadph Oxidase ◽  
Dependent Manner ◽  
Tubular Epithelial Cells ◽  
Mesenchymal Transition ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Diphenylene Iodonium ◽  
Renal Tubular

We examined whether and how uric acid induces epithelial to mesenchymal transition (EMT) in renal tubular cells, along with the mechanism by which telmisartan acts on uric acid-induced renal injury. Rat renal proximal tubular epithelial cells (NRK-52E) were exposed to various concentrations of uric acid in the presence or absence of telmisartan. Treatment with uric acid increased the expression of α-SMA, decreased the expression of E-cadherin, and promoted EMT in NRK-52E cells. Uric acid treatment also led to increased endothelin-1 (ET-1) production, activation of extracellular-regulated protein kinase 1/2 (ERK1/2), and the upregulation of nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4). Use of ET-1 receptor inhibitor (BQ123 or BQ788) could inhibit uric acid-induced EMT in NRK-52E cells. Pretreatment with the ERK inhibitor (U0126 or PD98059) suppressed the release of ET-1 and EMT induced by uric acid. Additionally, pretreatment with a traditional antioxidant (diphenylene iodonium or apocynin) inhibited the activation of ERK1/2, release of ET-1, and uric acid-induced EMT in NRK-52E cells. These findings suggested that uric acid-induced EMT in renal tubular epithelial cells occurs through NADPH oxidase-mediated ERK1/2 activation and the subsequent release of ET-1. Furthermore, telmisartan (102 nmol/L to 104 nmol/L) inhibited the expression of NOX4, intracellular reactive oxygen species (ROS), activation of ERK1/2, and the release of ET-1 in a dose-dependent manner, thereby preventing uric acid-induced EMT in NRK-52E. In conclusion, telmisartan could ameliorate uric acid-induced EMT in NRK-52E cells likely through inhibition of the NADPH oxidase/ERK1/2/ET-1 pathway.

scholarly journals Vitamin C attenuates the toxic effect of aristolochic acid on renal tubular cells via decreasing oxidative stress-mediated cell death pathways

2015 ◽  
Vol 12 (4) ◽  
pp. 6086-6092 ◽  
Author(s):  
TSAI-KUN WU ◽  
CHYOU-WEI WEI ◽  
YING-RU PAN ◽  
SHUR-HUEIH CHERNG ◽  
WEI-JUNG CHANG ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Vitamin C ◽  
Toxic Effect ◽  
Aristolochic Acid ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Cell Death Pathways ◽  
Renal Tubular

A Study of the Hypouricaemic Effect of Tiaprofenic Acid

1988 ◽  
Vol 25 (6) ◽  
pp. 595-600 ◽  
Author(s):  
Vivienne Lyfar ◽  
L Fernandes ◽  
Elizabeth Thornton ◽  
J G H Cook
Keyword(s):  
Uric Acid ◽  
Cell Membrane ◽  
Tiaprofenic Acid ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Acid Clearance ◽  
Uric Acid Clearance ◽  
Site Of Action ◽  
Extra Cellular Fluid ◽  
Renal Tubular

Tiaprofenic acid is a non-steroidal anti-inflammatory drug which also has hypouriceamic effect. Studies involving 10 healthy volunteers were designed to investigate the mode of this effect. We postulate that the site of action of tiaprofenic acid is at the cell membrane, the mechanism being an interference with the transport of uric acid from intra- to extra-cellular fluid thus limiting its passage into the plasma. The same mechanism acting on renal tubular cells impedes reabsorption thereby increasing uric acid clearance.

Reduction of Oxidative Stress in Cultured Renal Tubular Cells and Preventive Effects on Renal Stone Formation by the Bioflavonoid Quercetin

2008 ◽  
Vol 179 (4) ◽  
pp. 1620-1626 ◽  
Author(s):  
Hyoung Keun Park ◽  
Byong Chang Jeong ◽  
Mi-Kyung Sung ◽  
Mi-Young Park ◽  
Eun Young Choi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Stone ◽  
Stone Formation ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Preventive Effects

Examination of the anti-oxidative effect in renal tubular cells and apoptosis by oxidative stress

2005 ◽  
Vol 33 (4) ◽  
pp. 261-266 ◽  
Author(s):  
Yasunori Itoh ◽  
Takahiro Yasui ◽  
Atsushi Okada ◽  
Keiichi Tozawa ◽  
Yutaro Hayashi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Oxidative Effect

scholarly journals Nephroprotective Effects of N-Acetylcysteine Amide against Contrast-Induced Nephropathy through Upregulating Thioredoxin-1, Inhibiting ASK1/p38MAPK Pathway, and Suppressing Oxidative Stress and Apoptosis in Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Xuezhong Gong ◽  
Yiru Duan ◽  
Junli Zheng ◽  
Yiquan Wang ◽  
Guohua Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Contrast Induced Nephropathy ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
P38 Mapk Pathway ◽  
Thioredoxin 1 ◽  
Renal Tubular

Contrast-induced nephropathy (CIN) is a leading cause of hospital-acquired acute kidney injury (AKI) due to apoptosis induced in renal tubular cells. Our previous study demonstrated the novel N-acetylcysteine amide (NACA); the amide form of N-acetyl cysteine (NAC) prevented renal tubular cells from contrast-induced apoptosis through inhibiting p38 MAPK pathway in vitro. In the present study, we aimed to compare the efficacies of NACA and NAC in preventing CIN in a well-established rat model and investigate whether thioredoxin-1 (Trx1) and apoptosis signal-regulating kinase 1 (ASK1) act as the potential activator for p38 MAPK. NACA significantly attenuated elevations of serum creatinine, blood urea nitrogen, and biomarkers of AKI. At equimolar concentration, NACA was more effective than NAC in reducing histological changes of renal tubular injuries. NACA attenuated activation of p38 MAPK signal, reduced oxidative stress, and diminished apoptosis. Furthermore, we demonstrated that contrast exposure resulted in Trx1 downregulation and increased ASK1/p38 MAPK phosphorylation, which could be reversed by NACA and NAC. To our knowledge, this is the first report that Trx1 and ASK1 are involved in CIN. Our study highlights a renal protective role of NACA against CIN through modulating Trx1 and ASK1/p38 MAPK pathway to result in the inhibition of apoptosis among renal cells.

Sign in / Sign up

Export Citation Format

Share Document