Effects of apocynin and losartan treatment on renal oxidative stress in a rat model of calcium oxalate nephrolithiasis

Li, Chengyang; Deng, Yaoliang; Sun, Bei

doi:10.1007/s11255-009-9534-0

Cited by 18 publications

(15 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Nox have since been identified as the major source of ROS that sustains the up-regulation of MCP-1 and osteopontin in renal tubular epithelial cells in response to hyperoxaluria [137,138]. Administration of AT 1 R blockers such as candesartan or losartan in stone-forming rat models reduced Nox activity and crystal deposits in the renal interstitium, corroborating that not only do Noxes become activated in hyperoxaluria conditions, but that they also play a key role in stone formation [139,140]. As such, it is probable that oxidative stress through Nox-derived ROS is a major contributor of renal cell injury, epithelial cell adhesion to crystallites and stone formation.…”

Section: Kidney Stones (Nephrolithiasis)mentioning

confidence: 87%

“…Stone formation occurs in a precise manner to allow crystallization, nucleation, growth and aggregation of urinary crystals and renal cell injury is a critical event in allowing crystal-cell interaction. Direct inhibition of Nox activity with apocynin in Sprague-Dawley rats with ethelene glycol-or hydroxyl-L-proline (HLP)-induced hyperoxaluria reduced CaOx crystal deposits as well as the expression of renal injury and inflammatory markers [139,141]. Administration of AT 1 R blockers such as candesartan or losartan in stone-forming rat models reduced Nox activity and crystal deposits in the renal interstitium, corroborating that not only do Noxes become activated in hyperoxaluria conditions, but that they also play a key role in stone formation [139,140].…”

Section: Kidney Stones (Nephrolithiasis)mentioning

confidence: 99%

See 1 more Smart Citation

Nox and renal disease

2014

View full text Add to dashboard Cite

Since the first demonstration of Nox enzyme expression in the kidney in the early 1990s and the subsequent identification of Nox4, or RENOX, a decade later, it has become apparent that the Nox family of reactive oxygen species (ROS) generating enzymes plays an integral role in the normal physiological function of the kidney. As our knowledge of Nox expression patterns and functions in various structures and specialized cell types within the kidney grows, so does the realization that Nox-derived oxidative stress contributes significantly to a wide variety of renal pathologies through their ability to modify lipids and proteins, damage DNA and activate transcriptional programmes. Diverse studies demonstrate key roles for Nox-derived ROS in kidney fibrosis, particularly in settings of chronic renal disease such as diabetic nephropathy. As the most abundant Nox family member in the kidney, much emphasis has been placed on the role of Nox4 in this setting. However, an ever growing body of work continues to uncover key roles for other Nox family members, not only in diabetic kidney disease, but in a diverse array of renal pathological conditions. The objective of the present review is to highlight the latest novel developments in renal Nox biology with an emphasis not only on diabetic nephropathy but many of the other renal disease contexts where oxidative stress is implicated.

show abstract

Section: Kidney Stones (Nephrolithiasis)mentioning

confidence: 87%

Section: Kidney Stones (Nephrolithiasis)mentioning

confidence: 99%

Nox and renal disease

2014

View full text Add to dashboard Cite

show abstract

“…Our previous studies demonstrated that hyperoxaluria and crystal deposition induced the production of ROS and renal epithelial cells injury in a rat model of calcium oxalate nephrolithiasis [27, 28]. Mitochondria are generally the most common intracellular sources of ROS, and cellular injury is usually accompanied by the production of ROS [29].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Autophagy Attenuated Ethylene Glycol Induced Crystals Deposition and Renal Injury in a Rat Model of Nephrolithiasis

Liu

Xiang

et al. 2018

Kidney Blood Press Res

View full text Add to dashboard Cite

Background/Aims: Nephrolithiasis is a common and frequently occurring disease, its exact pathogenesis is remains unclear. Emerging data suggest that autophagy plays a vital role in the pathophysiological processes of kidney diseases. Therefore, this study was designed to investigate the potential role of autophagy in the formation of calcium oxalate (CaOx) kidney stones in rat model. Methods: Thirty-two rats were randomly divided into four groups (eight rats/group): untreated control group, stone model group, rapamycin-treated group, chloroquine-treated group. Rat models of CaOx nephrolithiasis was administration of 0.75% ethylene glycol (EG) in their drinking water for 4 weeks. Western blot and transmission electron microscope (TEM) were used to detect the expression of autophagy related protein LC3-II, BECN1 and p62 and autophagic vacuoles respectively. Renal function was evaluated by measuring the levels of serum CRE and BUN. Renal tubular injury markers NGAL and Kim-1 was determined by ELISA kits. Von Kossa staining was used to assess crystal deposits and histological tissue injury. TUNEL staining was employed to assess apoptosis of the renal tubular cell. Results: Compare with the controls, the expression of autophagy related protein LC3-II, BECN1 and number of autophagic vacuoles were increased significantly, whereas the p62 protein level was decreased in the stone model group. The levels of apoptosis, serum CRE and BUN, NGAL and Kim-1 in the stone model group were increased compared with the control group and crystals deposition and renal injury were increased significantly. However, the levels of autophagy, kidney injury and crystal deposition were decreased by chloroquine but increased by rapamycin. Conclusion: These findings suggested that rats were administration of ethylene glycol could lead to the formation of CaOx nephrolithiasis and autophagy activation. Inhibiting autophagy could be an effective therapeutic approach for decreasing the formation of nephrolithiasis.

show abstract

“…The source of ROS in tissue injury is largely dependent on the types of enzymes activated. The NOX family has been identified as a major source of superoxide and hydrogen peroxide in the kidney during health and disease [13,22,23,24,25]. NOX consists of at least one membrane-bound NOX/p22-phox complex and cytosolic subunits p67-phox, p47-phox, p40-phox as well as the small GTPase rac1 or rac2.…”

Section: Discussionmentioning

confidence: 99%

Involvement of NOX in the Regulation of Renal Tubular Expression of Na/K-ATPase in Acute Unilateral Ureteral Obstruction Rats

Liu

Song

Liu

et al. 2015

Nephron

View full text Add to dashboard Cite

Background/Aims: Renal tubular expression of Na/K-ATPase has been reported to be rapidly reduced in kidneys after unilateral ureteral obstruction (UUO), contributing to compromised sodium regulation. In this study, apocynin was utilized to test the hypothesis that the renal nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) system is involved in the regulation of Na/K-ATPase expression in early UUO. Methods: Eighty Wistar rats underwent UUO or sham surgery, and half of each group was administered 100 mg/kg apocynin by oral gavage after surgery. Renal tissue samples were collected on day 1 and day 3 after surgery and the distribution of NOX2, NOX4 and Na/K-ATPase was assessed by immunofluorescence and immunohistochemical staining. The Heme oxygenase-1 (HO-1), NOX2, NOX4, osteopontin, Na/K-ATPase and aquaporin-1 (AQP-1) content of renal homogenates was assessed by immunoblotting, and malondialdehyde (MDA), nitric oxide (NO) content was assessed by biochemical analyses. Activity of inducible NO synthase (iNOS) and antioxidant enzymes was assessed by enzymatic assay. Results: Kidney Na/K-ATPase and AQP-1 content was decreased, and MDA and NOX4, NOX2 and HO-1 content were increased in the obstructed kidneys of UUO rats. Apocynin attenuated these changes and partially, but significantly, reversed the downregulation of Na/K-ATPase and AQP-1 in UUO rats. However, apocynin did not alter iNOS activity and NO production, osteopontin expression or the activity of antioxidant enzymes. Conclusion: Activation of the NOX system and subsequent production of ROS are likely responsible for the downregulation of renal tubular Na/K-ATPase expression in early UUO.

show abstract

Effects of apocynin and losartan treatment on renal oxidative stress in a rat model of calcium oxalate nephrolithiasis

Abstract: These results suggest that renal Ang II and its stimulation of NADPH oxidase may partially account for the development of OS in kidney in this rat model of CaOx nephrolithiasis.

Cited by 18 publications

References 42 publications

Nox and renal disease

Nox and renal disease

Inhibition of Autophagy Attenuated Ethylene Glycol Induced Crystals Deposition and Renal Injury in a Rat Model of Nephrolithiasis

Involvement of NOX in the Regulation of Renal Tubular Expression of Na/K-ATPase in Acute Unilateral Ureteral Obstruction Rats

Contact Info

Product

Resources

About