Research Article

羟基柠檬酸通过降低氧化应激和炎症反应抑制肾脏草酸钙的沉积

卷 20, 期 7, 2020

页: [527 - 535] 页: 9

弟呕挨: 10.2174/1566524020666200103141116

价格: $65

摘要

目的:本研究旨在评估羟基柠檬酸(HCA)对乙醛酸酯诱导的小鼠模型结石的预防作用。 材料与方法:将雄性C57BL / 6J小鼠分为对照组,乙醛酸盐(GOX)100 mg / kg组,GOX + HCA 100 mg / kg组和GOX + HCA 200 mg / kg组。在实验的第八天收集血液样品和肾脏样品。我们使用Pizzolato染色和偏光显微镜检查晶体形成,并通过丙二醛(MDA),超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的水平评估氧化应激。定量逆转录聚合酶链反应(qRT-PCR)用于检测单核细胞趋化蛋白1(MCP-1),核因子κB(NFκB),白介素1β(IL-1β)的表达)和白介素6(IL-6)信使RNA(mRNA)。免疫组织化学和qRT-PCR检测骨桥蛋白(OPN)的表达和分化簇44(CD44)的表达。此外,高碘酸席夫(PAS)染色和TUNEL法用于评估肾小管损伤和细胞凋亡。 结果:HCA治疗可以减少肾功能损害的指标(血尿素氮和血清肌酐)。用HCA处理的小鼠中草酸钙晶体的沉积明显减少。草酸钙晶体诱导了活性氧的产生,并降低了抗氧化防御酶的活性。 HCA减弱了草酸钙结晶引起的氧化应激。 HCA对草酸钙诱导的炎症细胞因子(如MCP-1,IL-1β和IL-6)具有抑制作用。此外,HCA减轻了草酸钙晶体引起的肾小管损伤和细胞凋亡。 结论:HCA通过抗氧化和抗炎症作用抑制乙醛酸诱导的小鼠模型的肾脏损伤和草酸钙晶体沉积。

关键词: 羟甲酸,肾结晶,氧化应激,炎症,草酸钙结晶沉积,抗氧化。

[1]
Scales CD Jr, Smith AC, Hanley JM, Saigal CS. Urologic diseases in America project. Prevalence of kidney stones in the United States. Eur Urol 2012; 62(1): 160-5.
[http://dx.doi.org/10.1016/j.eururo.2012.03.052] [PMID: 22498635]
[2]
Wu W, Yang B, Ou L, et al. Urinary stone analysis on 12,846 patients: a report from a single center in China. Urolithiasis 2014; 42(1): 39-43.
[http://dx.doi.org/10.1007/s00240-013-0633-0] [PMID: 24362574]
[3]
Shoag J, Halpern J, Goldfarb DS, Eisner BH. Risk of chronic and end stage kidney disease in patients with nephrolithiasis. J Urol 2014; 192(5): 1440-5.
[http://dx.doi.org/10.1016/j.juro.2014.05.117] [PMID: 24929140]
[4]
Basavaraj DR, Biyani CS, Browning AJ, Cartledge JJ. The Role of urinary kidney stone inhibitors and promoters in the pathogenesis of calcium containing renal stones. EAU-EBU Update Ser 2007; 5: 126-36.
[http://dx.doi.org/10.1016/j.eeus.2007.03.002]
[5]
Joshi S, Wang W, Peck AB, Khan SR. Activation of the NLRP3 inflammasome in association with calcium oxalate crystal induced reactive oxygen species in kidneys. J Urol 2015; 193(5): 1684-91.
[http://dx.doi.org/10.1016/j.juro.2014.11.093] [PMID: 25437532]
[6]
Ma MC, Chen YS, Huang HS. Erythrocyte oxidative stress in patients with calcium oxalate stones correlates with stone size and renal tubular damage. Urology 2014; 83(2): 510.e9-510.e17.
[http://dx.doi.org/10.1016/j.urology.2013.09.050] [PMID: 24360074]
[7]
Taguchi K, Okada A, Kitamura H, et al. Colony-stimulating factor-1 signaling suppresses renal crystal formation. J Am Soc Nephrol 2014; 25(8): 1680-97.
[http://dx.doi.org/10.1681/ASN.2013060675] [PMID: 24578130]
[8]
Tang C, Dong Z. Mitochondria in Kidney Injury: When the power plant fails. J Am Soc Nephrol 2016; 27(7): 1869-72.
[http://dx.doi.org/10.1681/ASN.2015111277] [PMID: 26744487]
[9]
Hall AM, Schuh CD. Mitochondria as therapeutic targets in acute kidney injury. Curr Opin Nephrol Hypertens 2016; 25(4): 355-62.
[http://dx.doi.org/10.1097/MNH.0000000000000228] [PMID: 27166518]
[10]
Srivastava S, Sinha D, Saha PP, Marthala H, D’Silva P. Magmas functions as a ROS regulator and provides cytoprotection against oxidative stress-mediated damages. Cell Death Dis 2014.5e1394
[http://dx.doi.org/10.1038/cddis.2014.355] [PMID: 25165880]
[11]
Oh GS, Kim HJ, Choi JH, et al. Pharmacological activation of NQO1 increases NAD+ levels and attenuates cisplatin-mediated acute kidney injury in mice. Kidney Int 2014; 85(3): 547-60.
[http://dx.doi.org/10.1038/ki.2013.330] [PMID: 24025646]
[12]
Hirose M, Tozawa K, Okada A, et al. Glyoxylate induces renal tubular cell injury and microstructural changes in experimental mouse. Urol Res 2008; 36(3-4): 139-47.
[http://dx.doi.org/10.1007/s00240-008-0143-7] [PMID: 18542940]
[13]
Tsujihata M. Mechanism of calcium oxalate renal stone formation and renal tubular cell injury. Int J Urol 2008; 15(2): 115-20.
[http://dx.doi.org/10.1111/j.1442-2042.2007.01953.x] [PMID: 18269444]
[14]
Kawana H, Karaki H, Higashi M, et al. CD44 suppresses TLR-mediated inflammation. J Immunol 2008; 180(6): 4235-45.
[http://dx.doi.org/10.4049/jimmunol.180.6.4235] [PMID: 18322236]
[15]
Semwal RB, Semwal DK, Vermaak I, Viljoen A. A comprehensive scientific overview of Garcinia cambogia. Fitoterapia 2015; 102: 134-48.
[http://dx.doi.org/10.1016/j.fitote.2015.02.012] [PMID: 25732350]
[16]
Sripradha R, Magadi SG. Efficacy of garcinia cambogia on body weight, inflammation and glucose tolerance in high fat fed male wistar rats. J Clin Diagn Res 2015; 9(2): BF01-4.
[http://dx.doi.org/10.7860/JCDR/2015/12045.5577] [PMID: 25859449]
[17]
Amin KA, Kamel HH, Abd Eltawab MA. Protective effect of Garcinia against renal oxidative stress and biomarkers induced by high fat and sucrose diet. Lipids Health Dis 2011; 10: 6.
[http://dx.doi.org/10.1186/1476-511X-10-6] [PMID: 21235803]
[18]
Chung J, Granja I, Taylor MG, Mpourmpakis G, Asplin JR, Rimer JD. Molecular modifiers reveal a mechanism of pathological crystal growth inhibition. Nature 2016; 536(7617): 446-50.
[http://dx.doi.org/10.1038/nature19062] [PMID: 27501150]
[19]
Shara M, Ohia SE, Schmidt RE, et al. Physico-chemical properties of a novel (-)-hydroxycitric acid extract and its effect on body weight, selected organ weights, hepatic lipid peroxidation and DNA fragmentation, hematology and clinical chemistry, and histopathological changes over a period of 90 days. Mol Cell Biochem 2004; 260(1-2): 171-86.
[http://dx.doi.org/10.1023/B:MCBI.0000026069.53960.75] [PMID: 15228099]
[20]
Ohia SE, Opere CA, LeDay AM, Bagchi M, Bagchi D, Stohs SJ. Safety and mechanism of appetite suppression by a novel hydroxycitric acid extract (HCA-SX). Mol Cell Biochem 2002; 238(1-2): 89-103.
[http://dx.doi.org/10.1023/A:1019911205672] [PMID: 12349913]
[21]
Pizzolato P. Histochemical recognition of calcium oxalate. J Histochem Cytochem 1964; 12: 333-6.
[http://dx.doi.org/10.1177/12.5.333] [PMID: 14193854]
[22]
Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)). Method Methods 2001; 25(4): 402-8.
[http://dx.doi.org/10.1006/meth.2001.1262] [PMID: 11846609]
[23]
Okada A, Yasui T, Hamamoto S, et al. Genome-wide analysis of genes related to kidney stone formation and elimination in the calcium oxalate nephrolithiasis model mouse: detection of stone-preventive factors and involvement of macrophage activity. J Bone Miner Res 2009; 24(5): 908-24.
[http://dx.doi.org/10.1359/jbmr.081245] [PMID: 19113933]
[24]
Khan SR. Reactive oxygen species as the molecular modulators of calcium oxalate kidney stone formation: evidence from clinical and experimental investigations. J Urol 2013; 189(3): 803-11.
[http://dx.doi.org/10.1016/j.juro.2012.05.078] [PMID: 23022011]
[25]
Khan SR. Hyperoxaluria-induced oxidative stress and antioxidants for renal protection. Urol Res 2005; 33(5): 349-57.
[http://dx.doi.org/10.1007/s00240-005-0492-4] [PMID: 16292585]
[26]
Ceban E, Banov P, Galescu A, Botnari V. Oxidative stress and antioxidant status in patients with complicated urolithiasis. J Med Life 2016; 9(3): 259-62.
[PMID: 27974930]
[27]
Patel M, Yarlagadda V, Adedoyin O, et al. Oxalate induces mitochondrial dysfunction and disrupts redox homeostasis in a human monocyte derived cell line. Redox Biol 2018; 15: 207-15.
[http://dx.doi.org/10.1016/j.redox.2017.12.003] [PMID: 29272854]
[28]
Mulay SR, Kulkarni OP, Rupanagudi KV, et al. Calcium oxalate crystals induce renal inflammation by NLRP3-mediated IL-1β secretion. J Clin Invest 2013; 123(1): 236-46.
[http://dx.doi.org/10.1172/JCI63679] [PMID: 23221343]
[29]
Habibzadegah-Tari P, Byer KG, Khan SR. Reactive oxygen species mediated calcium oxalate crystal-induced expression of MCP-1 in HK-2 cells. Urol Res 2006; 34(1): 26-36.
[http://dx.doi.org/10.1007/s00240-005-0007-3] [PMID: 16397773]
[30]
Boonla C, Hunapathed C, Bovornpadungkitti S, et al. Messenger RNA expression of monocyte chemoattractant protein-1 and interleukin-6 in stone-containing kidneys. BJU Int 2008; 101(9): 1170-7.
[http://dx.doi.org/10.1111/j.1464-410X.2008.07461.x] [PMID: 18241247]
[31]
Yasui T, Okada A, Hamamoto S, et al. Pathophysiology-based treatment of urolithiasis. Int J Urol 2017; 24(1): 32-8.
[http://dx.doi.org/10.1111/iju.13187] [PMID: 27539983]
[32]
Khaskhali MH, Byer KJ, Khan SR. The effect of calcium on calcium oxalate monohydrate crystal-induced renal epithelial injury. Urol Res 2009; 37(1): 1-6.
[http://dx.doi.org/10.1007/s00240-008-0160-6] [PMID: 19005647]
[33]
Wesson JA, Ward MD. Role of crystal surface adhesion in kidney stone disease. Curr Opin Nephrol Hypertens 2006; 15(4): 386-93.
[http://dx.doi.org/10.1097/01.mnh.0000232879.50716.6f] [PMID: 16775453]
[34]
Khan SR. Role of renal epithelial cells in the initiation of calcium oxalate stones. Nephron, Exp Nephrol 2004; 98(2): e55-60.
[http://dx.doi.org/10.1159/000080257] [PMID: 15499208]
[35]
Asselman M, Verhulst A, De Broe ME, Verkoelen CF. Calcium oxalate crystal adherence to hyaluronan-, osteopontin-, and CD44-expressing injured/regenerating tubular epithelial cells in rat kidneys. J Am Soc Nephrol 2003; 14(12): 3155-66.
[http://dx.doi.org/10.1097/01.ASN.0000099380.18995.F7] [PMID: 14638914]
[36]
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. PLoS One 2013; 8(4)e61343
[http://dx.doi.org/10.1371/journal.pone.0061343] [PMID: 23630583]

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