MP20-13 OXYGEN NANO-BUBBLE WATER EXERTS INHIBITORY EFFECTS ON KIDNEY STONE FORMATION BY INHIBITING RENAL TUBULAR CELL INJURY

2014 ◽  
Vol 191 (4S) ◽  
Author(s):  
Yasuhiko Hirose ◽  
Kazumi Taguchi ◽  
Yasuhiro Fujii ◽  
Kazuhiro Niimi ◽  
Shuzo Hamamoto ◽  
...  
Keyword(s):  
Kidney Stone ◽  
Cell Injury ◽  
Stone Formation ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Inhibitory Effects ◽  
Renal Tubular ◽  
Kidney Stone Formation

2087 OXYGEN NANO-BUBBLE WATER EXERTS INHIBITORY EFFECTS ON KIDNEY STONE FORMATION BY PROTECTING RENAL TUBULAR CELL INJURY

2013 ◽  
Vol 189 (4S) ◽  
Author(s):  
Yasuhiko Hirose ◽  
Takahiro Yasui ◽  
Kazumi Taguchi ◽  
Kazuhiro Niimi ◽  
Shuzo Hamamoto ◽  
...  
Keyword(s):  
Kidney Stone ◽  
Cell Injury ◽  
Stone Formation ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Inhibitory Effects ◽  
Renal Tubular ◽  
Kidney Stone Formation

scholarly journals Metformin Prevents Renal Stone Formation through an Antioxidant Mechanism In Vitro and In Vivo

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Xiong Yang ◽  
Hao Ding ◽  
Zhenbang Qin ◽  
Changwen Zhang ◽  
Shiyong Qi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Injury ◽  
Mdck Cells ◽  
Stone Formation ◽  
Treated Group ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Renal Tubular

Oxidative stress is a causal factor and key promoter of urolithiasis associated with renal tubular epithelium cell injury. The present study was designed to investigate the preventive effects of metformin on renal tubular cell injury induced by oxalate and stone formation in a hyperoxaluric rat model. MTT assays were carried out to determine the protection of metformin from oxalate-induced cytotoxicity. The intracellular superoxide dismutase (SOD) activities and malondialdehyde (MDA) levels were measured in vitro. Male Sprague-Dawley rats were divided into control group, ethylene glycol (EG) treated group, and EG + metformin treated group. Oxidative stress and crystal formations were evaluated in renal tissues after 8-week treatment. Metformin significantly inhibited the decrease of the viability in MDCK cells and HK-2 cells induced by oxalate. Besides, metformin markedly prevented the increased concentration of MDA and the decreased tendency of SOD in oxalate-induced MDCK cells and HK-2 cells. In vivo, the increased MDA levels and the reduction of SOD activity were detected in the EG treated group compared with controls, while these parameters reversed in the EG + metformin treated group. Kidney crystal formation in the EG + metformin treated group was decreased significantly compared with the EG treated group. Metformin suppressed urinary crystal deposit formation through renal tubular cell protection and antioxidative effects.

Propylene glycol-induced proximal renal tubular cell injury

1997 ◽  
Vol 30 (1) ◽  
pp. 134-139 ◽  
Author(s):  
Peter D. Yorgin ◽  
Andreas A. Theodorou ◽  
Amira Al-Uzri ◽  
Karen Davenport ◽  
Leslie V. Boyer-Hassen ◽  
...  
Keyword(s):  
Propylene Glycol ◽  
Cell Injury ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Renal Tubular

scholarly journals HIF-1-mediated production of exosomes during hypoxia is protective in renal tubular cells

2017 ◽  
Vol 313 (4) ◽  
pp. F906-F913 ◽  
Author(s):  
Wei Zhang ◽  
Xiangjun Zhou ◽  
Qisheng Yao ◽  
Yutao Liu ◽  
Hao Zhang ◽  
...  
Keyword(s):  
Cell Injury ◽  
Hypoxia Inducible Factor ◽  
Atp Depletion ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Dependent Manner ◽  
Protective Effects ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular

Exosomes are nano-sized vesicles produced and secreted by cells to mediate intercellular communication. The production and function of exosomes in kidney tissues and cells remain largely unclear. Hypoxia is a common pathophysiological condition in kidneys. This study was designed to characterize exosome production during hypoxia of rat renal proximal tubular cells (RPTCs), investigate the regulation by hypoxia-inducible factor-1 (HIF-1), and determine the effect of the exosomes on ATP-depletion-induced tubular cell injury. Hypoxia did not change the average sizes of exosomes secreted by RPTCs, but it significantly increased exosome production in a time-dependent manner. HIF-1 induction with dimethyloxalylglycine also promoted exosome secretion, whereas pharmacological and genetic suppression of HIF-1 abrogated the increase of exosome secretion under hypoxia. The exosomes from hypoxic RPTCs had inhibitory effects on apoptosis of RPTCs following ATP depletion. The protective effects were lost in the exosomes from HIF-1α knockdown cells. It is concluded that hypoxia stimulates exosome production and secretion in renal tubular cells. The exosomes from hypoxic cells are protective against renal tubular cell injury. HIF-1 mediates exosome production during hypoxia and contributes to the cytoprotective effect of the exosomes.

A14340 Endothelial dysfunction exacerbates renal tubular cell injury through inflammasome activation in hypertensive model mice

2018 ◽  
Vol 36 ◽  
pp. e76
Author(s):  
Nagasu Hajime ◽  
Kengo Kidokoro ◽  
Minoru Satoh ◽  
Seiji Itano ◽  
Tamaki Sasaki ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Cell Injury ◽  
Tubular Cell ◽  
Inflammasome Activation ◽  
Renal Tubular Cell ◽  
Renal Tubular
Sign in / Sign up

Export Citation Format

Share Document