Use of intravoxel incoherent motion MRI to assess renal fibrosis in a rat model of unilateral ureteral obstruction

2016 ◽  
Vol 44 (3) ◽  
pp. 698-706 ◽  
Author(s):  
Xiang-Ran Cai ◽  
Juan Yu ◽  
Qing-Chun Zhou ◽  
Bin Du ◽  
You-Zhen Feng ◽  
...  
2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Dapeng Zhao ◽  
Zhongqiu Luan

Renal fibrosis is a common final pathological process in the progression of kidney disease. Oleanolic acid is a bioactive pentacyclic triterpenoid and is widely found in medicinal herbs around the world. In this study, we explored the effect of oleanolic acid on renal fibrosis and the underlying molecular mechanisms by using a rat model of unilateral ureteral obstruction (UUO). Male Sprague-Dawley rats were orally administered with oleanolic acid (6 mg/kg/d) or vehicle (olive oil) for 21 days after the UUO surgery. Upon termination, urine and blood were collected for renal function analysis, and kidneys were harvested for pathological analysis by using hematoxylin-eosin and Masson trichrome staining. Changes of extracellular matrix mRNA expressions and TGF-β/Smad signaling in the kidneys were also determined. As a result, oleanolic acid significantly reduced the kidney index, the level of serum creatinine and blood urea nitrogen, and the urinary level of microalbumin, α1-microglobulin, and N-acetyl-β-glucosaminidase. Masson trichrome staining showed significantly less collagen deposition in the UUO rats with oleanolic acid treatment. Diminished mRNA expressions of collagen I, collagen III, fibronectin, and α-SMA in the kidney tissues were observed after the treatment. Oleanolic acid led to decreased protein expressions of TGF-β, TGF-β receptor I, and TGF-β receptor II, as well as the phosphorylation of Smad2. Our current study suggested that oleanolic acid could be a complementary and alternative therapy for renal fibrosis potentially by targeting the TGF-β/Smad pathway.


2020 ◽  
Vol 41 (12) ◽  
pp. 1597-1608
Author(s):  
Ji-zhe Jin ◽  
Hui-ying Li ◽  
Jian Jin ◽  
Shang-guo Piao ◽  
Xiong-hu Shen ◽  
...  

2017 ◽  
Vol 31 (2) ◽  
pp. e3858 ◽  
Author(s):  
Maguelonne Pons ◽  
Benjamin Leporq ◽  
Liza Ali ◽  
Marianne Alison ◽  
Miguel Albuquerque ◽  
...  

PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0148542 ◽  
Author(s):  
Marilena Gregorini ◽  
Valeria Corradetti ◽  
Chiara Rocca ◽  
Eleonora Francesca Pattonieri ◽  
Teresa Valsania ◽  
...  

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Akito Maeshima ◽  
Keiichiro Mishima ◽  
Shin Yamashita ◽  
Masao Nakasatomi ◽  
Masaaki Miya ◽  
...  

Activin, a member of the TGF-βsuperfamily, regulates cell growth and differentiation in various cell types. Activin A acts as a negative regulator of renal development as well as tubular regeneration after renal injury. However, it remains unknown whether activin A is involved in renal fibrosis. To clarify this issue, we utilized a rat model of unilateral ureteral obstruction (UUO). The expression of activin A was significantly increased in the UUO kidneys compared to that in contralateral kidneys. Activin A was detected in glomerular mesangial cells and interstitial fibroblasts in normal kidneys. In UUO kidneys, activin A was abundantly expressed by interstitialα-SMA-positive myofibroblasts. Administration of recombinant follistatin, an activin antagonist, reduced the fibrotic area in the UUO kidneys. The number of proliferating cells in the interstitium, but not in the tubules, was significantly lower in the follistatin-treated kidneys. Expression ofα-SMA, deposition of type I collagen and fibronectin, and CD68-positive macrophage infiltration were significantly suppressed in the follistatin-treated kidneys. These data suggest that activin A produced by interstitial fibroblasts acts as a potent profibrotic factor during renal fibrosis. Blockade of activin A action may be a novel approach for the prevention of renal fibrosis progression.


Sign in / Sign up

Export Citation Format

Share Document