scholarly journals Amelioration of Cisplatin-Induced Acute Renal Injury by Renal Progenitor-Like Cells Derived from the Adult Rat Kidney

2008 ◽  
Vol 17 (1-2) ◽  
pp. 143-158 ◽  
Author(s):  
Masaru Kinomura ◽  
Shinji Kitamura ◽  
Katsuyuki Tanabe ◽  
Kunihiro Ichinose ◽  
Kumiko Hirokoshi ◽  
...  
2008 ◽  
Vol 179 (4S) ◽  
pp. 117-118
Author(s):  
Taro Iguchi ◽  
Manabu Nishikawa ◽  
Masayasu Inoue ◽  
Ching Y Wang ◽  
Gabriel P Haas ◽  
...  

2004 ◽  
Vol 38 (4) ◽  
pp. 333-341 ◽  
Author(s):  
Taro Iguchi ◽  
Manabu Nishikawa ◽  
BaoJun Chang ◽  
Osuke Muroya ◽  
Eisuke F sato ◽  
...  

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Zhiquan Xu ◽  
Xiaoyan Huang ◽  
Qiuyu Lin ◽  
Wei Xiang

Abstract Objective Long noncoding RNA (lncRNA) taurine upregulated gene 1 (TUG1) is increased under the condition of ischemia. This study intended to identify the mechanism of TUG1 in renal ischemia-reperfusion (I/R). Methods First, a rat model of acute renal injury induced by I/R was established, followed by the measurement of blood urea nitrogen (BUN), serum creatine (SCr), methylenedioxyphetamine (MDA) and superoxide dismutase (SOD) in the serum of rats. TUG1 was knocked down in I/R rats (ko-TUG1 group). Next, histological staining was used to evaluate the pathological damage and apoptosis of rat kidney. Western blot analysis was used to detect the levels of apoptosis- and autophagy-related proteins and transmission electron microscope was used to observe autophagosomes. Autophagy and apoptosis were evaluated after inhibition of the autophagy pathway using the inhibitor 3-MA. The targeting relation among TUG1, microRNA (miR)-29 and phosphatase and tensin homolog (PTEN) were validated. Lastly, the effects of TUG1 on biological behaviors of renal tubular cells were evaluated in vitro. Results In vivo, the levels of BUN, SCr and MDA in the serum of I/R-treated rats were increased while SOD level and autophagosomes were reduced, tubule epithelial cells were necrotic, and TUG1 was upregulated in renal tissues of I/R-treated rats, which were all reversed in rats in the ko-TUG1 group. Autophagy inhibition (ko-TUG1 + 3-MA group) averted the protective effect of TUG1 knockdown on I/R-treated rats. TUG1 could competitively bind to miR-29 to promote PTEN expression. In vitro, silencing TUG1 (sh-TUG1 group) promoted viability and autophagy of renal tubular cells and inhibited apoptosis. Conclusions LncRNA TUG can promote PTEN expression by competitively binding to miR-29 to promote autophagy and inhibited apoptosis, thus aggravating acute renal injury in I/R-treated rats.


2020 ◽  
pp. 1-1
Author(s):  
Rujittika Mungmunpuntipantip ◽  
Viroj Wiwanitkit

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Liu Tongqiang ◽  
Liu Shaopeng ◽  
Yu Xiaofang ◽  
Song Nana ◽  
Xu Xialian ◽  
...  

Contrast-induced acute renal injury (CI-AKI) has become a common cause of hospital-acquired renal failure. However, the development of prophylaxis strategies and approved therapies for CI-AKI is limited. Salvianolic acid B (SB) can treat cardiovascular-related diseases. The aim of the present study was to assess the effect of SB on prevention of CI-AKI and explore its underlying mechanisms. We examined its effectiveness of preventing renal injury in a novel CI-AKI rat model. Compared with saline, intravenous SB pretreatment significantly attenuated elevations in serum creatinine and the histological changes of renal tubular injuries, reduced the number of apoptosis-positive tubular cells, activated Nrf2, and lowered the levels of renal oxidative stress induced by iodinated contrast media. The above renoprotection of SB was abolished by the PI3K inhibitor (wortmannin). In HK-2 cells, SB activated Nrf2 and decreased the levels of oxidative stress induced by hydrogen peroxide and subsequently improved cell viability. The above cytoprotection of SB was blocked by the PI3K inhibitor (wortmannin) or siNrf2. Thus, our results demonstrate that, due to its antioxidant properties, SB has the potential to effectively prevent CI-AKI via the PI3K/Akt/Nrf2 pathway.


2014 ◽  
Vol 4 (1) ◽  
Author(s):  
Natalia O. Litbarg ◽  
Snezana Vujicic ◽  
Suman Setty ◽  
Periannan Sethupathi ◽  
George Dunea ◽  
...  

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