scholarly journals Protective Effect of 17β Estradiol against Kidney Injury in a Mouse Model of Unilateral Renal Ischemia

2021 ◽  
Vol 7 (1) ◽  
pp. 1-10
Author(s):  
Carolyn M Ecelbarger ◽  

Renal ischemia can lead to irreversible damage to the kidney including atrophy and fibrosis. Young females generally experience attenuated pathology due to the protective actions of ovarian steroids, in particular 17β-Estradiol (E2); however, the mechanisms of action remain murky.

Renal Failure ◽  
2019 ◽  
Vol 41 (1) ◽  
pp. 314-325 ◽  
Author(s):  
Warumphon Sukkummee ◽  
Patcharin Jittisak ◽  
Piyanuch Wonganan ◽  
Supeecha Wittayalertpanya ◽  
Pajaree Chariyavilaskul ◽  
...  

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e93297 ◽  
Author(s):  
Melissa A. Bellinger ◽  
James S. Bean ◽  
Melissa A. Rader ◽  
Kathleen M. Heinz-Taheny ◽  
Jairo S. Nunes ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Chuanfeng Lv ◽  
Tie Hong ◽  
Zhen Yang ◽  
Yu Zhang ◽  
Lu Wang ◽  
...  

In this paper, the protective effect of the bioflavonoid quercetin on behaviors, antioxidases, and neurotransmitters in 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine-(MPTP-) induced Parkinson's disease (PD) was investigated. Quercetin treatment (50 mg/kg, 100 mg/kg and 200 mg/kg body weight) was orally administered for 14 consecutive days. The results show that quercetin treatment markedly improves the motor balance and coordination of MPTP-treated mice. Significant increases were observed in the activities of glutathione peroxidase (GPx), superoxide dismutase (SOD), and Na+, K+-ATPase, AchE, the content of dopamine (DA) in the quercetin plus MPTP groups compared to those in the MPTP group. Significant reduction the 4-hydroxy-2-nonenal (4-HNE) immunoreactivity in striatum of brains was observed in the quercetin plus MPTP groups in comparison to the MPTP group. Taken together, we propose that quercetin has shown antiparkinsonian properties in our studies. More work is needed to explore detailed mechanisms of action.


Platelets ◽  
2018 ◽  
Vol 30 (2) ◽  
pp. 199-205 ◽  
Author(s):  
Xiuhua Li ◽  
Yusheng Li ◽  
Kan Shen ◽  
Hongqiang Li ◽  
Jianwen Bai

2012 ◽  
Vol 683 (1-3) ◽  
pp. 270-275 ◽  
Author(s):  
Ryosuke Tanaka ◽  
Hidenobu Tsutsui ◽  
Shuhei Kobuchi ◽  
Takahiro Sugiura ◽  
Masayo Yamagata ◽  
...  

2018 ◽  
Vol 40 (5) ◽  
pp. 423-429 ◽  
Author(s):  
Ali-Mohammad Rousta ◽  
Seyed-Mohamad-Sadegh Mirahmadi ◽  
Alireza Shahmohammadi ◽  
Davood Nourabadi ◽  
Mohammad-Reza Khajevand-Khazaei ◽  
...  

2016 ◽  
Vol 7 (1) ◽  
pp. 6 ◽  
Author(s):  
Mehdi Nematbakhsh ◽  
Nahid Talebi ◽  
Ramesh Monajemi ◽  
Safoora Mazaheri ◽  
Ardeshir Talebi ◽  
...  

2012 ◽  
Vol 303 (11) ◽  
pp. F1487-F1494 ◽  
Author(s):  
Qingqing Wei ◽  
Zheng Dong

Renal ischemia-reperfusion leads to acute kidney injury (AKI), a major kidney disease associated with an increasing prevalence and high mortality rates. A variety of experimental models, both in vitro and in vivo, have been used to study the pathogenic mechanisms of ischemic AKI and to test renoprotective strategies. Among them, the mouse model of renal clamping is popular, mainly due to the availability of transgenic models and the relatively small animal size for drug testing. However, the mouse model is generally less stable, resulting in notable variations in results. Here, we describe a detailed protocol of the mouse model of bilateral renal ischemia-reperfusion. We share the lessons and experiences gained from our laboratory in the past decade. We further discuss the technical issues that account for the variability of this model and offer relevant solutions, which may help other investigators to establish a well-controlled, reliable animal model of ischemic AKI.


2019 ◽  
Vol 317 (3) ◽  
pp. F616-F622 ◽  
Author(s):  
Jin Wei ◽  
Yingliang Wang ◽  
Jie Zhang ◽  
Lei Wang ◽  
Liying Fu ◽  
...  

Transplanted kidneys usually experience several episodes of ischemia, including cold ischemia during allograft storage in preservation solution. However, previous studies focusing on cold renal ischemia were only carried out in vitro or ex vivo. In the present study, we developed and characterized an in vivo mouse model of renal ischemia-reperfusion injury (IRI) induced exclusively by cold ischemia. C57BL/6 mice underwent right kidney nephrectomy, and the left kidney was kept cool with circulating cold saline in a kidney cup, while body temperature was maintained at 37°C. We clamped the renal pedicle and flushed out the blood inside the kidney with cold saline via an opening on the renal vein. The severity of renal IRI was examined with different ischemic durations. We found that the mice with <2 h of cold ischemia exhibited no significant changes in renal function or histopathology; animals with 3 or 4 h of cold ischemia developed into mild to moderate acute kidney injury with characteristic features, including the elevation in plasma creatinine concentration and reduction in glomerular filtration rate and tubular necrosis, followed by a subsequent recovery. However, mice with 5 h of cold ischemia died in a few days with severe acute kidney injury. In summary, we generated a mouse model of renal IRI induced exclusively by cold ischemia, which mimics graft cold storage in preservation solution, and renal function can be evaluated in vivo.


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