scholarly journals Exogenous pancreatic kininogenase protects against renal fibrosis in rat model of unilateral ureteral obstruction

2020 ◽  
Vol 41 (12) ◽  
pp. 1597-1608
Author(s):  
Ji-zhe Jin ◽  
Hui-ying Li ◽  
Jian Jin ◽  
Shang-guo Piao ◽  
Xiong-hu Shen ◽  
...  
Keyword(s):  
Rat Model ◽  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Unilateral Ureteral Obstruction

scholarly journals Oleanolic Acid Attenuates Renal Fibrosis through TGF-β/Smad Pathway in a Rat Model of Unilateral Ureteral Obstruction

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Dapeng Zhao ◽  
Zhongqiu Luan
Keyword(s):  
Oleanolic Acid ◽  
Rat Model ◽  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Function Analysis ◽  
Unilateral Ureteral Obstruction ◽  
Smad Pathway ◽  
Complementary And Alternative Therapy ◽  
Collagen Iii ◽  
Masson Trichrome Staining

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.

scholarly journals Mesenchymal Stromal Cells Prevent Renal Fibrosis in a Rat Model of Unilateral Ureteral Obstruction by Suppressing the Renin-Angiotensin System via HuR

PLoS ONE ◽  
2016 ◽  
Vol 11 (2) ◽  
pp. e0148542 ◽  
Author(s):  
Marilena Gregorini ◽  
Valeria Corradetti ◽  
Chiara Rocca ◽  
Eleonora Francesca Pattonieri ◽  
Teresa Valsania ◽  
...  
Keyword(s):  
Mesenchymal Stromal Cells ◽  
Rat Model ◽  
Stromal Cells ◽  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Renin Angiotensin System ◽  
Unilateral Ureteral Obstruction ◽  
Angiotensin System ◽  
Renin Angiotensin

scholarly journals Follistatin, an Activin Antagonist, Ameliorates Renal Interstitial Fibrosis in a Rat Model of Unilateral Ureteral Obstruction

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Akito Maeshima ◽  
Keiichiro Mishima ◽  
Shin Yamashita ◽  
Masao Nakasatomi ◽  
Masaaki Miya ◽  
...  
Keyword(s):  
Rat Model ◽  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Type I Collagen ◽  
Interstitial Fibrosis ◽  
Activin A ◽  
Unilateral Ureteral Obstruction ◽  
Negative Regulator ◽  
Type I ◽  
Glomerular Mesangial Cells

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.

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 ◽  
...  
Keyword(s):  
Rat Model ◽  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Unilateral Ureteral Obstruction ◽  
Intravoxel Incoherent Motion ◽  
Motion Mri

scholarly journals NLRP3 Deficiency Attenuates Renal Fibrosis and Ameliorates Mitochondrial Dysfunction in a Mouse Unilateral Ureteral Obstruction Model of Chronic Kidney Disease

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Honglei Guo ◽  
Xiao Bi ◽  
Ping Zhou ◽  
Shijian Zhu ◽  
Wei Ding
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Mitochondrial Dysfunction ◽  
Ureteral Obstruction ◽  
Renal Fibrosis ◽  
Unilateral Ureteral Obstruction ◽  
Tubulointerstitial Fibrosis ◽  
Mitochondrial Morphology ◽  
Glomerular Injury ◽  
Matrix Deposition

Background and Aims. The nucleotide-binding domain and leucine-rich repeat containing PYD-3 (NLRP3) inflammasome has been implicated in the pathogenesis of chronic kidney disease (CKD); however, its exact role in glomerular injury and tubulointerstitial fibrosis is still undefined. The present study was performed to identify the function of NLRP3 in modulating renal injury and fibrosis and the potential involvement of mitochondrial dysfunction in the murine unilateral ureteral obstruction (UUO) model of CKD. Methods. Employing wild-type (WT) and NLRP3−/− mice with or without UUO, we evaluated renal structure, tissue injury, and mitochondrial ultrastructure, as well as expression of some vital molecules involved in the progression of fibrosis, apoptosis, inflammation, and mitochondrial dysfunction. Results. The severe glomerular injury and tubulointerstitial fibrosis induced in WT mice by UUO was markedly attenuated in NLRP3−/− mice as evidenced by blockade of extracellular matrix deposition, decreased cell apoptosis, and phenotypic alterations. Moreover, NLRP3 deletion reversed UUO-induced impairment of mitochondrial morphology and function. Conclusions. NLRP3 deletion ameliorates mitochondrial dysfunction and alleviates renal fibrosis in a murine UUO model of CKD.

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