Erythropoietin Attenuates Renal Injury in an Experimental Model of Rat Unilateral Ureteral Obstruction via Anti-Inflammatory and Anti-Apoptotic Effects

Chang, Yoon-Kyung; Choi, Dae Eun; Na, Ki Young; Lee, Sang-Ju; Suh, Kwang Sun; Kim, Suk Young; Shin, Young-Tai; Lee, Kang Wook

doi:10.1016/j.juro.2008.10.105

Cited by 30 publications

(29 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study, renal IRI increased the levels of Bcl-2, Bax and cleaved Caspase3, while NADPH treatment reduced these phenotypes. A similar observation was found in that Bcl-2 and Bax were mainly localized in renal tubular cells, and that levels of Bcl-2 and Bax were remarkably increased in IRI kidneys compared with the sham group [42]. However, Na et al observed that Bax expression was significantly elevated, and that Bcl-2 expression was decreased in IR kidney [24].…”

Section: Discussionsupporting

confidence: 67%

Protective Effect of Nicotinamide Adenine Dinucleotide Phosphate on Renal Ischemia-Reperfusion Injury

Weng

Song

et al. 2018

Kidney Blood Press Res

View full text Add to dashboard Cite

Background/Aims: Renal ischemia-reperfusion injury (IRI) is a common consequence of acute kidney injury. Nicotinamide adenine dinucleotide phosphate (NADPH), which is derived from the pentose phosphate pathway, is essential for the proper functioning of essential redox and antioxidant defense systems. Previous studies have indicated that NADPH is responsible for protecting the brain from ischemic injury. The goal of this study was to analyze the protective function of NADPH in renal IRI. Methods: The IRI animal model was generated through a midline laparotomy surgery that clamped both sides of the renal pedicles for 40 min to induce renal ischemia. The in vitro model was generated by removing oxygen and glucose from human kidney epithelial cells (HK-2 cells), followed by reoxygenation to imitate IRI. Renal function and histopathological changes were observed and evaluated. Additionally, malondialdehyde and glutathione levels were determined in renal tissue homogenate as indicators of oxidative stress. ROS production in cells was determined by DHE staining. Protein biomarker expression was evaluated by western blot, apoptosis was analyzed by TUNEL staining, and p65 nuclear translocation was visualized by immunofluorescence. Results: Our data indicated that NADPH safeguarded the kidneys from histological and functional damage, and significantly reduce cell injury along with preventing potential increases in blood urea nitrogen and creatinine levels. Furthermore, we observed that NADPH increased glutathione levels, while reducing levels of malondialdehyde and reactive oxygen species. Additionally, our results suggested that NADPH treatment may alleviate IRI-induced apoptosis and inflammation. Conclusion: NADPH treatment may protect against renal IRI and should be further developed as a new treatment for acute kidney injury.

show abstract

Section: Discussionsupporting

confidence: 67%

Protective Effect of Nicotinamide Adenine Dinucleotide Phosphate on Renal Ischemia-Reperfusion Injury

Weng

Song

et al. 2018

Kidney Blood Press Res

View full text Add to dashboard Cite

show abstract

“…The plasma was separated by centrifugation (10 min, 4°C), and aliquots were snap-frozen in liquid nitrogen and stored at -70°C. Tissues were prepared as previously described [24]. Briefly, the left kidney was excised immediately after sacrifice and cut into three coronal sections.…”

Section: Blood and Tissue Preparationmentioning

confidence: 99%

“…Immunohistochemistry Immunohistochemistry was performed as described previously [24]. Paraffin wax-embedded tissues were cut into 4 µm sections, mounted on glass slides, and stained using indirect immunoperoxidase.…”

Section: Light Microscopymentioning

confidence: 99%

Co-inhibition of Angiotensin II Receptor and Endothelin-1 Attenuates Renal Injury in Unilateral Ureteral Obstructed Mice

Chang

Choi

Jeong

et al. 2016

Kidney Blood Press Res

Self Cite

View full text Add to dashboard Cite

Background/Aims: Both endothelin-1 (ET-1) and the renin-angiotensin system (RAS) may play important roles in renal fibrosis in the obstructed kidney. However, there have been few clear demonstrations of a relationship between their activation and additive or synergistic roles in renal fibrosis. We investigated the protective roles and relationship between renal RAS and ET-1 in unilateral ureteral obstruction (UUO) mice. Methods: 8-week-old male C57BL/6 mice were divided into seven groups: sham, bosentan+sham, valsartan+sham, vehicle+UUO, bosentan+UUO, valsartan+UUO, and valsartan+bosentan+UUO. Valsartan and bosentan were administered orally using an NG tube (valsartan 10 mg/kg/day, bosentan 100 mg/kg/day for 8 days, after which the molecular and structural kidney parameters were evaluated. Bosentan treatment elevated plasma renin activity, renal renin, and AT1R expression in UUO mice. Results: Although valsartan decreased plasma ET-1 in these mice, it did not affect ET(A) or ET(B) in their kidneys. Co-treatment with valsartan and bosentan decreased ET-1 in these mice compared to the single treatments. Bosentan, but not valsartan, elevated eNOS expression in their kidneys. Co-treatment with valsartan and bosentan reduced TGF-β, α-SMA, and collagen IV expression, and the Masson's trichrome stained area in their kidneys. Conclusions: Bosentan and valsartan acted complementarily, and co-treatment with both drugs had an additive protective effect against renal fibrosis.

show abstract

“…22,23 The third possible mechanism is the inhibitory effect of EPO on inflammation and fibrosis. Attenuation of interstitial inflammation and fibrosis by EPO therapy has been reported in the models of chronic cyclosporine nephropathy, 24 ureteral obstruction, [25][26][27] and Thy-1 glomerulonephritis. 28 In addition, other mechanisms have been suggested to be involved in the direct renoprotective effect of EPO.…”

Section: Discussionmentioning

confidence: 93%

Erythropoiesis-stimulating agent slows the progression of chronic kidney disease: a possibility of a direct action of erythropoietin

et al. 2016

View full text Add to dashboard Cite

Background Controversy exists regarding the renoprotective effect of erythropoiesis-stimulating agent (ESA) in progressive chronic kidney disease (CKD) with renal anemia. In this study, we examined whether ESA therapy has a renoprotective effect in progressive CKD. Methods The subjects in this retrospective observational study were 68 non-dialysis dependent CKD patients with renal anemia. We compared the progression rate (PR), defined by the slope of the linear regression line of estimated glomerular filtration rate, measured during 6 months just before and after the start of ESA therapy. We also investigated the factors affecting renoprotective efficacy of ESA therapy against the progression of CKD. Results Median (interquartile range) PR decreased significantly from 6.2 (3.7-12.7) to 4.0 (À0.3 to 7.3) mL/min/1.73 m

show abstract

Erythropoietin Attenuates Renal Injury in an Experimental Model of Rat Unilateral Ureteral Obstruction via Anti-Inflammatory and Anti-Apoptotic Effects

Abstract: Erythropoietin exerts renoprotective effects in an experimental unilateral ureteral obstruction rat model via anti-apoptotic and anti-inflammatory actions.

Cited by 30 publications

References 19 publications

Protective Effect of Nicotinamide Adenine Dinucleotide Phosphate on Renal Ischemia-Reperfusion Injury

Protective Effect of Nicotinamide Adenine Dinucleotide Phosphate on Renal Ischemia-Reperfusion Injury

Co-inhibition of Angiotensin II Receptor and Endothelin-1 Attenuates Renal Injury in Unilateral Ureteral Obstructed Mice

Erythropoiesis-stimulating agent slows the progression of chronic kidney disease: a possibility of a direct action of erythropoietin

Contact Info

Product

Resources

About