-
摘要: 烟酰胺腺嘌呤二核苷酸磷酸(NADPH)氧化酶(NOX)在肾炎症反应、缺血/再灌注损伤、肾小管上皮细胞和肾脏间质细胞损伤的病理生理过程中起着关键性的作用。该酶激活后产生大量氧自由基(ROS)参与多种细胞内信号转导,引发炎性反应,细胞损伤等过程。过量的ROS将导致肾损伤、成石物质沉积、肾结石的形成及肾功能衰竭等病理生理改变。NOX抑制剂可以有效改善上述病理过程。本综述旨在讨论NOX在肾结石形成过程中的作用以及NOX抑制剂的肾脏保护作用。Abstract: Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase plays a crucial role in renal inflammation, ischemia/reperfusion injury and the injury of renal tubular epithelial cells and interstitial cells. After being activated, the enzyme produces large amounts of reactive oxygen species (ROS) which are involved in various intracellular signal transduction, leading to inflammatory response and cell injury. Excess ROS will lead to kidney damage, deposition of stone material, the formation of kidney stones, renal failure and other pathophysiological changes. NADPH oxidase inhibitor can effectively improve the above mentioned pathological process. The purpose of this review is to study the role of NADPH oxidase in the formation of kidney stones as well as NADPH oxidase inhibitors in renal protection.
-
Key words:
- NADPH oxidase /
- nephrolithiasis /
- reactive oxygen species /
- research progress
-
-
[1] Zeng Q, He Y. Age-specific prevalence of kidney stones in Chinese urban inhabitants[J]. Urolithiasis, 2013, 41(1):91-93.
[2] Khan S R. Reactive oxygen species, inflammation and calcium oxalate nephrolithiasis[J]. Transl Androl Urol, 2014, 3(3):256-276.
[3] Khan S R. Stress oxidative:nephrolithiasis and chronic kidney diseases[J]. Minerva Med, 2013, 104(1):23-30.
[4] Kodama R, Kato M, Furuta S, et al. ROS-generating oxidases Nox1 and Nox4 contribute to oncogenic Ras-induced premature senescence[J]. Genes Cells, 2013, 18(1):32-41.
[5] San Martin A, Griendling K K. NADPH oxidases:progress and opportunities[J]. Antioxid Redox Signal, 2014, 20(17):2692-2694.
[6] Liu X, Pei C, Yan S, et al. NADPH oxidase 1-dependent ROS is crucial for TLR4 signaling to promote tumor metastasis of non-small cell lung cancer[J]. Tumour Biol, 2015.
[7] Karimi G, Houee Levin C, Dagher M C, et al. Assembly of phagocyte NADPH oxidase:A concerted binding process[J]? Biochim Biophys Acta, 2014, 1840(11):3277-3283.
[8] Marciano B E, Spalding C, Fitzgerald A, et al. Common severe infections in chronic granulomatous disease[J]. Clin Infect Dis, 2014.
[9] Verzola D, Ratto E, Villaggio B, et al. Uric AUric acid promotes apoptosis in human proximal tubule cells by oxidative stress and the activation of NADPH oxidase NOX 4[J]. PLoS One, 2014, 9(12):e115210.
[10] Sun L, Li W, Xiong L, et al. Astragaloside IV prevents damage to human mesangial cells through the inhibition of the NADPH oxidase/ROS/Akt/NFkappaB pathway under high glucose conditions[J]. Int J Mol Med, 2014, 34(1):167-176.
[11] Joshi S, Peck A B, Khan S R. NADPH oxidase as a therapeutic target for oxalate induced injury in kidneys[J]. Oxid Med Cell Longev, 2013, 2013:462361.
[12] Holterman C E, Thibodeau J F, Kennedy C R. NADPH oxidase 5 and renal disease[J]. Curr Opin Nephrol Hypertens, 2015, 24(1):81-87.
[13] Chen S, Meng X F, Zhang C. Role of NADPH oxidase-mediated reactive oxygen species in podocyte injury[J]. Biomed Res Int, 2013, 2013:839761.
[14] Khan S R. Reactive oxygen species as the molecular modulators of calcium oxalate kidney stone formation:evidence from clinical and experimental investigations[J]. J Urol, 2013, 189(3):803-811.
[15] Khan A, Byer K, Khan S R. Exposure of Madin-Darby canine kidney (MDCK) cells to oxalate and calcium oxalate crystals activates nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase[J]. Urology, 2014, 83(2):510,e511-517.
[16] Umekawa T, Tsuji H, Uemura H, et al. 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[J]. BJU Int, 2009, 104(1):115-120.
[17] Yeh C C, Chang J Z, Yang W H, et al. NADPH oxidase 4 is involved in the triethylene glycol dimethacrylate-induced reactive oxygen species and apoptosis in human embryonic palatal mesenchymal and dental pulp cells[J]. Clin Oral Investig, 2015, 19(6):1463-1471.
[18] Fujii Y, Okada A, Yasui T, et al. Effect of adiponectin on kidney crystal formation in metabolic syndrome model mice via inhibition of inflammation and apoptosis[J]. PLoS One, 2013, 8(4):e61343.
[19] Liang L, Li L, Tian J, et al. Androgen receptor enhances kidney stone-CaOx crystal formation via modulation of oxalate biosynthesis & oxidative stress[J]. Mol Endocrinol, 2014, 28(8):1291-1303.
[20] Khan S R, Joshi S, Wang W, et al. Regulation of macromolecular modulators of urinary stone formation by reactive oxygen species:transcriptional study in an animal model of hyperoxaluria[J]. Am J Physiol Renal Physiol, 2014, 306(11):F1285-1295.
[21] Pragasam V, Sakthivel R, Kalaiselvi P, et al.Detection of endothelial nitric oxide synthase and NADPH-diaphorase in experimentally induced hyperoxaluric animals[J]. Urol Res, 2005, 33(4):301-308.
[22] Tsujihata M, Yoshioka I, Tsujimura A, et al. Why does atorvastatin inhibit renal crystal retention[J]? Urol Res, 2011, 39(5):379-383.
[23] Li C Y, Deng Y L, Sun B H. Effects of apocynin and losartan treatment on renal oxidative stress in a rat model of calcium oxalate nephrolithiasis[J]. Int Urol Nephrol, 2009, 41(4):823-833.
[24] Joshi S, Wang W, Peck A B, et al. Activation of the NLRP3 inflammasome in association with calcium oxalate crystal induced reactive oxygen species in kidneys[J]. J Urol, 2015, 193(5):1684-1691.
[25] Carrasco A Jr, Granberg C F, Gettman M T,et al. Surgical management of stone disease in patients with primary hyperoxaluria[J]. Urology, 2015, 85(3):522-526.
[26] Richman K, O'Bell J, Pareek G. The growing prevalence of kidney stones and opportunities for prevention[J]. R I Med J (2013), 2014, 97(12):31-34.
[27] Wu Y X, Li C Y, Deng Y L. Patients with nephrolithiasis had lower fetuin-A protein level in urine and renal tissue[J]. Urolithiasis, 2014, 42(1):29-37.
[28] Zhuang Y, Feng Q, Ding G, et al. Activation of ERK1/2 by NADPH oxidase-originated reactive oxygen species mediates uric acid-induced mesangial cell proliferation[J]. Am J Physiol Renal Physiol, 2014, 307(4):F396-406.
[29] Sanchez-Lozada L G, Soto V, Tapia E, et al. Role of oxidative stress in the renal abnormalities induced by experimental hyperuricemia[J]. Am J Physiol Renal Physiol, 2008, 295(4):F1134-1141.
[30] Kuo F C, Tseng Y T, Wu S R, et al. Melamine activates NFkappaB/COX-2/PGE2 pathway and increases NADPH oxidase-dependent ROS production in macrophages and human embryonic kidney cells[J]. Toxicol In Vitro, 2013, 27(6):1603-1611.
[31] Li X, Lu J, Shang P, et al. The selective NADPH oxidase inhibitor apocynin has potential prophylactic effects on melamine-related nephrolithiasis in vitro and in vivo[J]. Mol Cell Biochem, 2015, 399(1-2):167-178.
[32] Chandasana H, Chhonker Y S, Bala V, et al. Pharmacokinetic, bioavailability, metabolism and plasma protein binding evaluation of NADPH-oxidase inhibitor apocynin using LC-MS/MS[J]. J Chromatogr B Analyt Technol Biomed Life Sci, 2015, 985:180-188.
[33] Ciarcia R, Damiano S, Florio A, et al. The protective effect of Apocynin on Cyclosporine A-induced hypertension and nephrotoxicity in rats[J]. J Cell Biochem, 2015, 116(9):1848-1856.
[34] Zuo J, Khan A, Glenton P A, et al. Effect of NADPH oxidase inhibition on the expression of kidney injury molecule and calcium oxalate crystal deposition in hydroxy-L-proline-induced hyperoxaluria in the male Sprague-Dawley rats[J]. Nephrol Dial Transplant, 2011, 26(6):1785-1796.
[35] Selemidis S, Sobey C G, Wingler K, et al. NADPH oxidases in the vasculature:molecular features, roles in disease and pharmacological inhibition[J]. Pharmacol Ther, 2008, 120(3):254-291.
[36] Umekawa T, Byer K, Uemura H, et al. Diphenyleneiodium (DPI) reduces oxalate ion- and calcium oxalate monohydrate and brushite crystal-induced upregulation of MCP-1 in NRK 52E cells[J]. Nephrol Dial Transplant, 2005, 20(5):870-878.
[37] Hong S H, Lee H J, Sohn E J, et al. Anti-nephrolithic potential of resveratrol via inhibition of ROS, MCP-1, hyaluronan and osteopontin in vitro and in vivo[J]. Pharmacol Rep, 2013, 65(4):970-979.
[38] Lee H J, Jeong S J, Park M N, et al. Gallotannin suppresses calcium oxalate crystal binding and oxalate-induced oxidative stress in renal epithelial cells[J]. Biol Pharm Bull, 2012, 35(4):539-544.
[39] Browatzki M, Larsen D, Pfeiffer C A, et al. Angiotensin II stimulates matrix metalloproteinase secretion in human vascular smooth muscle cells via nuclear factor-kappaB and activator protein 1 in a redox-sensitive manner[J]. J Vasc Res, 2005, 42(5):415-423.
[40] Cupisti A, D'Alessandro C, Samoni S, et al. Nephrolithiasis and hypertension:possible links and clinical implications[J]. J Nephrol, 2014, 27(5):477-482.
[41] Yoshioka I, Tsujihata M, Akanae W, et al. Angiotensin type-1 receptor blocker candesartan inhibits calcium oxalate crystal deposition in ethylene glycol-treated rat kidneys[J]. Urology, 2011, 77(4):1007.e9-1007.e14.
-
计量
- 文章访问数: 133
- PDF下载数: 105
- 施引文献: 0