Catechin prevents the calcium oxalate monohydrate induced renal calcium crystallization in NRK-52E cells and the ethylene glycol induced renal stone formation in rat

BMC Complementary and Alternative Medicine

Yunfei Xu¹  Guangchun Wang¹  Jianhua Huang¹  Min Liu¹  Bo Peng¹  Xudong Yao¹  Junhua Zheng¹  Wei Zhai¹ 

[1]Department of Urology, Shanghai Tenth People’s Hospital, Tongji University School of Medicine, Shanghai 200072, China

关键词: In vitro;    In vivo;    Catechin;    Renal calcium crystallization;    Renal tubular cell injury;   

Others  :  1220992
DOI  :  10.1186/1472-6882-13-228

 received in 2013-03-20, accepted in 2013-08-28,  发布年份 2013

【 摘 要 】

Background

Reactive oxygen species play important roles in renal calcium crystallization. In this study, we examined the effects of catechin, which have been shown to have antioxidant properties on the renal calcium crystallization.

Methods

In the vitro experiment, the changes of the mitochondrial membrane potential, expression of superoxide dismutase (SOD), 4-hydroxynonenal (4-HNE), cytochrome c, and cleaved caspase 3 were measured to show the effects of catechin treatment on the NRK-52E cells induced by calcium oxalate monohydrate (COM). In the vivo study, Sprague–Dawley rats were administered 1% ethylene glycol (EG) to generate a rat kidney stone model and then treated with catechin (2.5 and 10 mg/kg/day) for 14 days. The urine and serum variables were dected on 7 and 14 days after EG administration. The expression of cytochrome c, cleaved caspase 3, SOD, osteopontin (OPN), malondialdehyde (MDA), 8-hydroxy-2′-deoxyguanosine (8-OHdG) in kidney were measured. Furthermore, the mitochondrial microstructure in the kidney was also examined by transmission electron microscopy.

Results

Catechin treatment could prevent the changes in mitochondrial membrane potential and expression of SOD, 4-HNE, cytochrome c, and cleaved caspase 3 in NRK-52E cells induced by the COM. For the in vivo experiments, the EG administration induced renal calcium crystallization was also prevented by the catechin. The expression of SOD, OPN, MDA, OPN and 8-OHdG, were increased after EG administration and this increase was diminished by catechin. Moreover, catechin also prevented EG induced mitochondrial collapse in rat.

Conclusions

Catechin has preventive effects on renal calcium crystallization both in vivo and in vitro, and provide a potential therapeutic treatment for this disease.

【 授权许可】

   
2013 Zhai et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

Figure 3.

Figure 4.

Figure 5.

Figure 6.

Figure 7.

【 参考文献 】

• [1]Byer K, Khan SR: Citrate provides protection against oxalate and calcium oxalate crystal induced oxidative damage to renal epithelium. J Urol 2005, 173:640-646.
• [2]Goodman HO, Brommage R, Assimos DG, Holmes RP: Genes in idiopathic calcium oxalate stone disease. World J Urol 1997, 15:186-194.
• [3]Vezzoli G, Terranegra A, Rainone F, Arcidiacono T, Cozzolino M, Aloia A, Dogliotti E, Cusi D, Soldati L: Calcium-sensing receptor and calcium kidney stones. J Transl Med 2011, 9:201. BioMed Central Full Text
• [4]Khan SR: Role of renal epithelial cells in the initiation of calcium oxalate stones. Nephron Exp Nephrol 2004, 98:e55-e60.
• [5]Thamilselvan S, Byer KJ, Hackett RL, Khan SR: Free radical scavengers, catalase and superoxide dismutase provide protection from oxalate-associated injury to LLC-PK1 and MDCK cells. J Urol 2000, 164:224-229.
• [6]Kohjimoto Y, Kennington L, Scheid CR, Honeyman TW: Role of phospholipase A2 in the cytotoxic effects of oxalate in cultured renal epithelial cells. Kidney Int 1999, 56:1432-1441.
• [7]Umekawa T, Byer K, Uemura H, Khan SR: Diphenyleneiodium (DPI) reduces oxalate ion- and calcium oxalate monohydrate and brushite crystal-induced upregulation of MCP-1 in NRK 52E cells. Nephrol Dial Transplant 2005, 20:870-878.
• [8]van de Water B, Zoeteweij JP, de Bont HJ, Mulder GJ, Nagelkerke JF: Role of mitochondrial Ca2+ in the oxidative stress-induced dissipation of the mitochondrial membrane potential. Studies in isolated proximal tubular cells using the nephrotoxin 1,2-dichlorovinyl-L-cysteine. J Biol Chem 1994, 269:14546-14552.
• [9]Kawai Y, Nakao T, Kunimura N, Kohda Y, Gemba M: Relationship of intracellular calcium and oxygen radicals to Cisplatin-related renal cell injury. J Pharmacol Sci 2006, 100:65-72.
• [10]Khan SR: Crystal-induced inflammation of the kidneys: results from human studies, animal models, and tissue-culture studies. Clin Exp Nephrol 2004, 8:75-88.
• [11]Nakamoto K, Takayama F, Mankura M, Hidaka Y, Egashira T, Ogino T, Kawasaki H, Mori A: Beneficial effects of fermented green tea extract in a rat model of non-alcoholic steatohepatitis. J Clin Biochem Nutr 2009, 44:239-246.
• [12]Khan SR: Reactive oxygen species as the molecular modulators of calcium oxalate kidney stone formation: evidence from clinical and experimental investigations. J Urol 2012, 189:83-811.
• [13]Kawabata T, Ma Y, Yamador I, Okada S: Iron-induced apoptosis in mouse renal proximal tubules after an injection of a renal carcinogen, iron-nitrilotriacetate. Carcinogenesis 1997, 18:1389-1394.
• [14]El-Sharaky AS, Newairy AA, Badreldeen MM, Eweda SM, Sheweita SA: Protective role of selenium against renal toxicity induced by cadmium in rats. Toxicology 2007, 235:185-193.
• [15]Poovala VS, Kanji VK, Tachikawa H, Salahudeen AK: Role of oxidant stress and antioxidant protection in acephate-induced renal tubular cytotoxicity. Toxicol Sci 1998, 46:403-409.
• [16]Wang C, Salahudeen AK: Cyclosporine nephrotoxicity: attenuation by an antioxidant-inhibitor of lipid peroxidation in vitro and in vivo. Transplantation 1994, 58:940-946.
• [17]Salahudeen A, Poovala V, Parry W, Pande R, Kanji V, Ansari N, Morrow J, Roberts J 2nd: Cisplatin induces N-acetyl cysteine suppressible F2-isoprostane production and injury in renal tubular epithelial cells. J Am Soc Nephrol 1998, 9:1448-1455.
• [18]Baliga R, Ueda N, Walker PD, Shah SV: Oxidant mechanisms in toxic acute renal failure. Am J Kidney Dis 1997, 29:465-477.
• [19]Servais H, Ortiz A, Devuyst O, Denamur S, Tulkens PM, Mingeot-Leclercq MP: Renal cell apoptosis induced by nephrotoxic drugs: cellular and molecular mechanisms and potential approaches to modulation. Apoptosis 2008, 13:11-32.
• [20]Kaushal GP, Basnakian AG, Shah SV: Apoptotic pathways in ischemic acute renal failure. Kidney Int 2004, 66:500-506.
• [21]Brooks C, Wei Q, Cho SG, Dong Z: Regulation of mitochondrial dynamics in acute kidney injury in cell culture and rodent models. J Clin Invest 2009, 119:1275-1285.
• [22]Porter AG, Janicke RU: Emerging roles of caspase-3 in apoptosis. Cell Death Differ 1999, 6:99-104.
• [23]Salvesen GS: Caspases: opening the boxes and interpreting the arrows. Cell Death Differ 2002, 9:3-5.
• [24]Ghavami S, Hashemi M, Ande SR, Yeganeh B, Xiao W, Eshraghi M, Bus CJ, Kadkhoda K, Wiechec E, Halayko AJ, Los M: Apoptosis and cancer: mutations within caspase genes. J Med Genet 2009, 46:497-510.
• [25]Katunuma N, Matsui A, Le QT, Utsumi K, Salvesen G, Ohashi A: Novel procaspase-3 activating cascade mediated by lysoapoptases and its biological significances in apoptosis. Adv Enzyme Regul 2001, 41:237-250.
• [26]Li P, Nijhawan D, Wang X: Mitochondrial activation of apoptosis. Cell 2004, 116:S57-S59. 52 p following S59
• [27]Cabrera C, Artacho R, Gimenez R: Beneficial effects of green tea–a review. J Am Coll Nutr 2006, 25:79-99.
• [28]Higdon JV, Frei B: Tea catechins and polyphenols: health effects, metabolism, and antioxidant functions. Crit Rev Food Sci Nutr 2003, 43:89-143.
• [29]Chander V, Singh D, Chopra K: Catechin, a natural antioxidant protects against rhabdomyolysis-induced myoglobinuric acute renal failure. Pharmacol Res 2003, 48:503-509.
• [30]Hase M, Babazono T, Karibe S, Kinae N, Iwamoto Y: Renoprotective effects of tea catechin in streptozotocin- induced diabetic rats. Int Urol Nephrol 2006, 38:693-699.
• [31]Chennasamudram SP, Kudugunti S, Boreddy PR, Moridani MY, Vasylyeva TL: Renoprotective effects of (+)-catechin in streptozotocin-induced diabetic rat model. Nutr Res 2012, 32:347-356.
• [32]Jeong BC, Kim BS, Kim JI, Kim HH: Effects of green tea on urinary stone formation: an in vivo and in vitro study. J Endourol 2006, 20:356-361.
• [33]Umekawa T, Tsuji H, Uemura H, Khan SR: Superoxide from NADPH oxidase as second messenger for the expression of osteopontin and monocyte chemoattractant protein-1 in renal epithelial cells exposed to calcium oxalate crystals. BJU Int 2009, 104:115-120.
• [34]Baines CP: The molecular composition of the mitochondrial permeability transition pore. J Mol Cell Cardiol 2009, 46:850-857.
• [35]Singh D, Chander V, Chopra K: Protective effect of catechin on ischemia-reperfusion-induced renal injury in rats. Pharmacol Rep 2005, 57:70-76.
• [36]Selvam R: Calcium oxalate stone disease: role of lipid peroxidation and antioxidants. Urol Res 2002, 30:35-47.
• [37]Thamilselvan S, Hackett RL, Khan SR: Lipid peroxidation in ethylene glycol induced hyperoxaluria and calcium oxalate nephrolithiasis. J Urol 1997, 157:1059-1063.
• [38]Khan SR, Thamilselvan S: Nephrolithiasis: a consequence of renal epithelial cell exposure to oxalate and calcium oxalate crystals. Mol Urol 2000, 4:305-312.
• [39]Niimi K, Yasui T, Hirose M, Hamamoto S, Itoh Y, Okada A, Kubota Y, Kojima Y, Tozawa K, Sasaki S, et al.: Mitochondrial permeability transition pore opening induces the initial process of renal calcium crystallization. Free Radic Biol Med 2012, 52:1207-1217.
• [40]Draper HH, Hadley M: Malondialdehyde determination as index of lipid peroxidation. Methods Enzymol 1990, 186:421-431.
• [41]Jonassen JA, Cao LC, Honeyman T, Scheid CR: Mechanisms mediating oxalate-induced alterations in renal cell functions. Crit Rev Eukaryot Gene Expr 2003, 13:55-72.
• [42]Sumitra K, Pragasam V, Sakthivel R, Kalaiselvi P, Varalakshmi P: Beneficial effect of vitamin E supplementation on the biochemical and kinetic properties of Tamm-Horsfall glycoprotein in hypertensive and hyperoxaluric patients. Nephrol Dial Transplant 2005, 20:1407-1415.
• [43]Huang HS, Ma MC, Chen J, Chen CF: Changes in the oxidant-antioxidant balance in the kidney of rats with nephrolithiasis induced by ethylene glycol. J Urol 2002, 167:2584-2593.
• [44]Kohri K, Nomura S, Kitamura Y, Nagata T, Yoshioka K, Iguchi M, Yamate T, Umekawa T, Suzuki Y, Sinohara H, et al.: Structure and expression of the mRNA encoding urinary stone protein (osteopontin). J Biol Chem 1993, 268:15180-15184.
• [45]Kohri K, Suzuki Y, Yoshida K, Yamamoto K, Amasaki N, Yamate T, Umekawa T, Iguchi M, Sinohara H, Kurita T: Molecular cloning and sequencing of cDNA encoding urinary stone protein, which is identical to osteopontin. Biochem Biophys Res Commun 1992, 184:859-864.
• [46]Wesson JA, Johnson RJ, Mazzali M, Beshensky AM, Stietz S, Giachelli C, Liaw L, Alpers CE, Couser WG, Kleinman JG, Hughes J: Osteopontin is a critical inhibitor of calcium oxalate crystal formation and retention in renal tubules. J Am Soc Nephrol 2003, 14:139-147.
• [47]Steitz SA, Speer MY, McKee MD, Liaw L, Almeida M, Yang H, Giachelli CM: Osteopontin inhibits mineral deposition and promotes regression of ectopic calcification. Am J Pathol 2002, 161:2035-2046.
• [48]Yamate T, Kohri K, Umekawa T, Iguchi M, Kurita T: Osteopontin antisense oligonucleotide inhibits adhesion of calcium oxalate crystals in Madin-Darby canine kidney cell. J Urol 1998, 160:1506-1512.
• [49]Kumar V, Penade la Vega L, Farell G, Lieske JC: Urinary macromolecular inhibition of crystal adhesion to renal epithelial cells is impaired in male stone formers. Kidney Int 2005, 68:1784-1792.
• [50]Okada A, Nomura S, Saeki Y, Higashibata Y, Hamamoto S, Hirose M, Itoh Y, Yasui T, Tozawa K, Kohri K: Morphological conversion of calcium oxalate crystals into stones is regulated by osteopontin in mouse kidney. J Bone Miner Res 2008, 23:1629-1637.