Diphenyleneiodium (DPI) reduces oxalate ion- and calcium oxalate monohydrate and brushite crystal-induced upregulation of MCP-1 in NRK 52E cells

Umekawa, Tohru; Byer, Karen J.; Uemura, Hirotsugu; Khan, Saeed R.

doi:10.1093/ndt/gfh750

Cited by 50 publications

(63 citation statements)

References 28 publications

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“…The concentration of oxalate in the urine changes as it moves through the nephron and is 0.22 mM in normal excreted urine, 0.44 mM in conditions of mild hyperoxaluria, and 1.5 mM in primary hyperoxaluria. Various studies have used 0.1-4 mM oxalate [30][31][32] for exposure of renal epithelial cells in vitro.…”

Section: Discussionmentioning

confidence: 99%

In vitro inhibition of calcium oxalate crystallization and crystal adherence to renal tubular epithelial cells by Terminalia arjuna

et al. 2015

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Urolithiasis is a multifactorial disease and remains a public health problem around the world. Of all types of renal stones, calcium oxalate (CaOx) is the most common composition formed in the urinary system of the patients with urolithiasis. The present study is aimed at evaluating the antiurolithiatic properties of the Tris-Cl extract (TE) of Terminalia arjuna (T. arjuna). The antilithiatic activity of TE of T. arjuna was investigated on nucleation, aggregation, and growth of the CaOx crystals, as well as its protective potency was tested on oxalate-induced cell injury of NRK-52E renal epithelial cells. Also, in vitro antioxidant activity of TE T. arjuna bark was also determined. The TE of T. arjuna exhibited a concentration-dependent inhibition of nucleation and growth of CaOx crystals. Inhibition of aggregation of CaOx crystals remains constant. When NRK-52E cells were injured by exposure to oxalate for 48 h, the TE prevented the cells from injury and CaOx crystal adherence resulting in increased cell viability in a dose-dependent manner. The TE also scavenged the 2,2-diphenyl-1-picrylhydrazyl (DPPH) free radicals with an IC50 at 51.72 µg/mL. The results indicated that T. arjuna is a potential candidate for phytotherapy against urolithiasis as it attains the ability to inhibit CaOx crystallization and scavenge DPPH free radicals in vitro along with a cytoprotective role.

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Section: Discussionmentioning

confidence: 99%

In vitro inhibition of calcium oxalate crystallization and crystal adherence to renal tubular epithelial cells by Terminalia arjuna

et al. 2015

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“…We propose that Ox and/or CaOx crystals may induce oxidative stress in kidneys and lead to an increased production of free radical, resulting in cell damage or cell death in renal tissue; however, this hypothesis should be tested by further studies. Then, crystal retention can be promoted due to increased exposure of crystal attachment sites as a result of tubular cell detachment or membrane structure alteration after oxalate and/or crystal injury, as proposed previously [26][27][28].…”

Section: Discussionmentioning

confidence: 87%

Renal tubular injury induced by ischemia promotes the formation of calcium oxalate crystals in rats with hyperoxaluria

et al. 2016

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Hyperoxaluria and cell injury are key factors in urolithiasis. Oxalate metabolism may be altered by renal dysfunction and therefore, impact the deposition of calcium oxalate (CaOx) crystals. We investigated the relationship of renal function, oxalate metabolism and CaOx crystal deposition in renal ischemia. One hundred male Sprague-Dawley rats were randomly divided into four groups. Hyperoxaluria model (Group A and B) was established by feeding rats with 0.75 % ethylene glycol (EG). The left renal pedicle was clamped for 30 min to establish renal ischemia Groups (B and C), while Groups A and D underwent sham operation. Then, serum and urine oxalate (Ox), creatinine (Cr) and urea nitrogen (UN) levels were evaluated by liquid chromatography mass spectrometry (LCMS) and ion mass spectrum (IMS) at days 0, 2, 4, 7, and 14. CaOx crystallization was assessed by transmission electron microscope (TEM). A temporal and significant increase of serum Cr and UN levels was observed in Groups B and C compared to values obtained for Groups A and D (P < 0.05). Ox levels in serum and urine were significantly higher in Groups A and B than in the other two groups from day 7 (P < 0.05). In addition, CaOx crystallization was observed in both Groups A and B, but Group B showed earlier and more pronounced crystal deposition in the renal tissue. Our results indicated that renal tubular injury induced by renal ischemia might not affect Ox levels but could promote CaOx crystal retention under hyperoxaluria.

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“…The attraction of inflammatory cells is thought to be caused by chemotactic proteins. The over-production of MCP-1 chemokine and IL-6 cytokine by crystal-exposed renal tubular cells was reported [10][11][12][13][14]16]. We hypothesized that MCP-1 and IL-6 were up-regulated in the kidney of patients with stones, and their increased contributed to renal dysfunction.…”

Section: Discussionmentioning

confidence: 91%

“…Evidence from cell-culture models confirmed that MCP-1 was up-regulated in renal tubular cell lines challenged with oxalate ions/ crystals, and its expression was attenuated by antioxidants [10][11][12][13][14]. Furthermore, there was crystal-induced up-regulation of MCP-1 and osteopontin in renal fibroblast cells [15].…”

Section: Introductionmentioning

confidence: 90%

Messenger RNA expression of monocyte chemoattractant protein‐1 and interleukin‐6 in stone‐containing kidneys

et al. 2008

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OBJECTIVESTo investigate the intrarenal mRNA expression of monocyte chemoattractant protein‐1 (MCP‐1) and interleukin‐6 (IL‐6) in patients with nephrolithiasis, and to evaluate whether their expression is associated with renal function, as oxidative stress and inflammation are involved in the pathogenesis of nephrolithiasis.PATIENTS, SUBJECTS AND METHODSRenal biopsies from near the stone, and blood and 24‐h urine specimens were collected from 29 patients with nephrolithiasis. Control renal tissues were taken from non‐cancerous and cancerous portions of nephrectomy from six patients with renal cancers, and control 24‐h urine samples were obtained from 30 healthy subjects. Corrected creatinine clearance, urinary N‐acetyl‐β‐glucosaminidase activity and 8‐hydroxy‐deoxyguanosine (8‐OHdG) were determined. The mRNA expressions of MCP‐1 and IL‐6 in the tissues were measured by real time reverse transcription‐polymerase chain reaction.RESULTSPatients with nephrolithiasis had significantly greater renal tubular damage and oxidative stress than the healthy controls. Intrarenal mRNA expressions of MCP‐1 and IL‐6 in stone‐adjacent renal tissues were significantly lower than in cancerous renal tissues, but not statistically different from that in non‐cancerous renal tissues. In stone‐adjacent renal tissues, the mRNA level of MCP‐1 was significantly higher than that of IL‐6, but their expressions were significantly correlated with each other. Histological examination showed that the number of infiltrated leukocytes corresponded well with the intrarenal mRNA levels of MCP‐1 and IL‐6. Patients with nephrolithiasis and compromised renal function had significantly higher intrarenal mRNA levels of MCP‐1 and IL‐6 than those with preserved renal function. Also, the mRNA levels in patients with severe renal tubular damage were significantly greater than in those with less renal tubular damage. There was no association between intrarenal mRNA expression and urinary 8‐OHdG.CONCLUSIONNephrolithiasis was associated with low‐grade intrarenal inflammation. A greater intrarenal mRNA expression of MCP‐1 and IL‐6 was associated with enhanced renal impairment. Thus, expression of MCP‐1 and IL‐6, at least in part, contributed to the progression of nephrolithiasis.

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Diphenyleneiodium (DPI) reduces oxalate ion- and calcium oxalate monohydrate and brushite crystal-induced upregulation of MCP-1 in NRK 52E cells

Cited by 50 publications

References 28 publications

In vitro inhibition of calcium oxalate crystallization and crystal adherence to renal tubular epithelial cells by Terminalia arjuna

In vitro inhibition of calcium oxalate crystallization and crystal adherence to renal tubular epithelial cells by Terminalia arjuna

Renal tubular injury induced by ischemia promotes the formation of calcium oxalate crystals in rats with hyperoxaluria

Messenger RNA expression of monocyte chemoattractant protein‐1 and interleukin‐6 in stone‐containing kidneys

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