钙化性纳米微粒与人肾小管上皮细胞相互作用研究
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摘要
目的观察体外细胞培养体系中人肾小管上皮细胞与钙化性纳米微粒的相互作用,探讨钙化性纳米微粒对人肾小管上皮细胞的损伤机制,探讨钙化性纳米微粒在肾结石形成中的可能作用。
方法体外建立人肾小管上皮细胞与钙化性纳米微粒共同培养体系,并使用NADPH氧化酶抑制剂apocynin进行干预处理。分别运用光镜、电镜观察人肾小管上皮细胞在与钙化性纳米微粒相互作用过程中的形态变化。实验分为四组,采用比色法测定24h后各组细胞培养液中乳酸脱氢酶、丙二醛、透明质酸的含量,同时检测细胞内NADPH氧化酶活性,采用RT-PCR测定各实验组细胞NADPH氧化酶亚基p22phox和p47phox mRNA的表达情况。
结果钙化性纳米微粒在体外能导致人肾小管上皮细胞的形态学改变,通过电子显微镜观察到人肾小管上皮细胞能够吸附、吞噬钙化性纳米微粒。钙化性纳米微粒也能导致人肾小管上皮细胞NADPH氧化酶p22phox、p47phox亚基mRNA的表达明显增强,同时伴有细胞氧化应激(oxidative stress,OS)损伤,使用apocynin干预后上述基因表达减少,同时细胞的氧化应激损伤也减轻。
结论在体外人肾小管上皮细胞具有粘附、吞噬钙化性纳米微粒的能力;钙化性纳米微粒能够引起人肾小管上皮细胞NADPH氧化酶的活性增强,导致细胞的氧化应激损伤。
Objective To observe the interaction of the calcifying nanoparticles (CNP) with human renal tubular epithelial cells (HK-2) in vitro. To investigate the mechanisms of HK-2 damage incited by CNP, and to investigate the potential role of CNP in the formation of nephrolithiasis.
Methods Human renal tubular epithelial cells were cultured with CNP in vitro, and the morphology changes was observed by light microscopy and electron microscopy. To investigate the oxidative stress, NADPH oxidase inhibitor apocynin was chosed as the intervention treatment. The levels of LDH, MDA, HA in the mediums and the activity of NADPH oxidase in human renal tubular epithelial cells were assessed after 24 hours. The expression of NADPH oxidase subunit p22phox and p47phox mRNA were detected by real-time quantitative PCR (RT-PCR).
Results CNP can cause morphology changes of the HK-2, have observed the adhesion and phagocytosis of CNP by the HK-2 under TEM. After 24 hours, the level of LDH, MDA, HA were significantly different among the 4 groups (P <0.05).
Conclusion HK-2 has abilities of adhering and phagocyting with CNP; and CNP can cause the damage induced by oxidative stress of HK-2.
方法体外建立人肾小管上皮细胞与钙化性纳米微粒共同培养体系,并使用NADPH氧化酶抑制剂apocynin进行干预处理。分别运用光镜、电镜观察人肾小管上皮细胞在与钙化性纳米微粒相互作用过程中的形态变化。实验分为四组,采用比色法测定24h后各组细胞培养液中乳酸脱氢酶、丙二醛、透明质酸的含量,同时检测细胞内NADPH氧化酶活性,采用RT-PCR测定各实验组细胞NADPH氧化酶亚基p22phox和p47phox mRNA的表达情况。
结果钙化性纳米微粒在体外能导致人肾小管上皮细胞的形态学改变,通过电子显微镜观察到人肾小管上皮细胞能够吸附、吞噬钙化性纳米微粒。钙化性纳米微粒也能导致人肾小管上皮细胞NADPH氧化酶p22phox、p47phox亚基mRNA的表达明显增强,同时伴有细胞氧化应激(oxidative stress,OS)损伤,使用apocynin干预后上述基因表达减少,同时细胞的氧化应激损伤也减轻。
结论在体外人肾小管上皮细胞具有粘附、吞噬钙化性纳米微粒的能力;钙化性纳米微粒能够引起人肾小管上皮细胞NADPH氧化酶的活性增强,导致细胞的氧化应激损伤。
Objective To observe the interaction of the calcifying nanoparticles (CNP) with human renal tubular epithelial cells (HK-2) in vitro. To investigate the mechanisms of HK-2 damage incited by CNP, and to investigate the potential role of CNP in the formation of nephrolithiasis.
Methods Human renal tubular epithelial cells were cultured with CNP in vitro, and the morphology changes was observed by light microscopy and electron microscopy. To investigate the oxidative stress, NADPH oxidase inhibitor apocynin was chosed as the intervention treatment. The levels of LDH, MDA, HA in the mediums and the activity of NADPH oxidase in human renal tubular epithelial cells were assessed after 24 hours. The expression of NADPH oxidase subunit p22phox and p47phox mRNA were detected by real-time quantitative PCR (RT-PCR).
Results CNP can cause morphology changes of the HK-2, have observed the adhesion and phagocytosis of CNP by the HK-2 under TEM. After 24 hours, the level of LDH, MDA, HA were significantly different among the 4 groups (P <0.05).
Conclusion HK-2 has abilities of adhering and phagocyting with CNP; and CNP can cause the damage induced by oxidative stress of HK-2.
引文
1.叶章群,邓耀良,董诚等.主编:泌尿系结石(第2版).北京:人民卫生出版社, 2010.
2. Kajander EO. Nanobacteria-propagating calcifying nanoparticles[J]. Lett Appl Microbiol, 2006, 42(6): 549-552.
3. Hjelle JT, Miller-Hjelle MA, Poxton IR. Endotoxin and nanobactera in polycystic kidney disease[J]. Kidney Int, 2000, 57(6): 2360-2374.
4. Sommer A, Oron U, Pretorius AM, et al. A preliminary investigation into light- modulated replication of nanobacteria and heart disease [J]. J Clin Laser Med & Surg, 2003, 21(4): 23l-235.
5. Puskas LG, Tiszlavicz L. Detection of nanobacteria like particles in human atherosclerotic plaques [J]. Acta Biol Hung, 2005, 56(3～4): 233-245.
6. WEN Yu, LI Yongguo, YANG Zhulin, et al. Nanobacteria in serum, bile and gallbladder mucosa of cholecystolithiasis patients [J]. Zhonghua Wai Ke Za Zhi, 2003, 4l(4): 267-270.
7. Turgut Demir. Is there any relation of nanobacteria with periodontal diseases [J]? Medical Hypotheses, 2008, 70, 36-39.
8. ZHOU Zhansong, LI Hong, SHEN Xuecheng, et al. Detection of nanobacteria infection in typeШprostatitis [J]. Urology, 2008, 71(6): 1091-1095.
9.唐中华,吴唯,吕新生,等.乳腺癌组织中钙化性纳米微粒样颗粒的电镜观察[J].医学临床研究, 2002, 19(3): 214-215.
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11. Hudelist G, Singer CF, Kubista E, et al. Presence of nanobacteria in psammoma bodies of ovarian cancer: evidence for pathogenetic role in intratumoral biomineralization [J]. Histopathology, 2004, 45(6): 633-637.
12. Ciftcioglu N, Kajander EO. Interaction of nanobacteria with cultured mammalian cells [J]. Pathophysiology, 1998, 4 (3): 259-270.
13. Coe FL, Evan A, Worcester E. Kidney stone disease. J Clin Invest. 2005, 115(10): 2598-2608.
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18. Kajander EO, Ciftcioglu N. Nanobacteria: an alternative mechanism for pathogenic intra-and extracellular calcification and stone formation. Proc Natl Acad Sci USA, 1998, 95(14): 8274-8279.
19. Kajander EO, Ciftcioglu N, Aho K, et al. Characteristics of nanobacteria and their possible role in stone formation [J]. Urol Res, 2003, 31 (2): 47-54.
20.陶芝伟,邓耀良,黎承杨.利用电镜技术对尿路钙化性纳米微粒的初步观察[J].广西医科大学学报, 2009, 26(6): 837-839.
21. Young JD, Martel J, Young L, et al. Putative nanobacteria represent physiological remnants and culture by-products of normal calcium homeostasis [J]. PLoS One, 2009, 4(2): e4417.
22. Young JD, Martel J, Young D, et al. Characterization of granulations of calcium and apatite in serum as pleomorphic mineralo-protein complexes and as precursors of putative nanobacteria [J]. PLoS One, 2009, 4(5): e5421.
23. Saldeen J. Cytokines induce both necrosis and apoptosis via a common Bcl-2 inhibitable pathway in rat insulin-producing cells. Endocrinology, 2000, 141(6): 2003-2010.
24. Peart J, Willems L, Headrick JP. Receptor and non-receptor-dependent mechanisms of cardioprotection with adenosine. Am J Physiol Heart Circ Physiol, 2003, 284(2): 519-527.
25. Scheid C, Koul H, Hill WA et al. Oxalate toxicity in LLC-PK1 cells, a line ofrenal epithelial cells. J Uro1, 1996, 15 5: 1112-1116.
26. Thamilselvan S, Hackett RL, and Khan SR. Lipid peroxidation in ethylene glycol induced hyperoxaluria and calcium oxalate nephrolithiasis. J Uro1, 1997, 157: 1059-1063.
27. Khand FD, Gordge MP- Robertson WC, et al. Mitochondrial superoxide production during oxalate mediated oxidative stress in renal epithelial ce1ls.Free Radic Biol Med, 2002, 32: 1339-1350.
28. Asaba K, Tojo A, Onozato et al. Effects of NADPH oxidase inhibitor in diabetic nephropathy. Kidney Int, 2005, 67:1890-1898.
29. Engels F, Renirie BF, Hart BA,et al. Effects of apocynin, a drug isolated from the roots of Picrorhiza kurroa, on arachidonic acid metabolism. FEBS Lett, 1992, 305:254-256.
30.司徒镇强,吴军正.细胞培养.西安:世界图书出版公司,2004, 250-252.
31. Danielyan I, Mueller L, Proksch B, et al. Similar protective effects of BQ-123 and erythropoietin on survival of neural cells and generation of neurons upon hypoxic injury. Eur J Cell Biol, 2005, 84(11): 907-913
32. Carrier RL, Ma TC, Obrietan K, et al. A sensitive and selective assay of neuronal degeneration in cell culture. J Neurosci Methods, 2006, 154(1-2):239-244.
33. Huang HS, Ma MC, Chen CF, et al. Lipid peroxidation and its correlations with urinary levels of oxalate, citric acid, and ostepopontin in patients with renal calcium oxalate stones[J]. Urology, 2003, 62(6): 1123-1128.
34. Tungsange K, Sriboonlue P, Futrakul P, et al. Renal tubular cell damage and oxidative stress in renal stone patients and the effect of potassium citrate treatment[J]. Urol Res, 2005, 33(1): 65-69.
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36. Tsuiihata M. Mechanism of calcium oxalate renal atone formation and renal tubular cell injury. Int J Uml, 2008, 15: 115-120.
37. Khan SR. Renal tubular damage/dysfunction: key to the formation of kidney stones. Urol Res, 2006, 34: 86-91.
38. Crystal-induced inflammation of the kidneys, results of human, animal model and tissue culture studies. Clin Exp Nephrol, 2004, 8: 75-88.
39.关晓峰,邓耀良,黎承杨,等.巨噬细胞在高草酸尿症大鼠肾内结石晶体形成过程中的作用[J].中华泌尿外科杂志,2010,31(2):88-91.
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41. Nagata M. Inflammatory cells and oxygen radicals. Curr Drug Targets Inflamm Allergy, 2005, 4(4): 503-504.
42. Victor VM, Rocha M, Esplugues JV, et al. Role of free radicals in sepsis: antioxidant therapy. Curr Pharm Des, 2005, 11(24):3141-3158.
43. 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 .Nephrology Dialysis Transplantation, 2005, 20: 870-878.
44. Rashed T, Menon M, Thamilselvan S. Molecular mechanism of oxalate-induced free radical production and glutathione redox imbalance in renal epithelial cells: effect of antioxidants. Am J Nephrol, 2004, 24: 557-568.
45. Li CY, Deng YL, Sun BH. Taurine protected kidney from oxidative injury through mitochondrial-linked pathway in a rat model of nephrolithiasis [J]. Urol Res, 2009, 37(4): 211-220.
46. Li CY, Deng YL, Sun BH. 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.
47. Hannken T, Schroeder R, Stahl RA, et al. Angiotensin II-mediated expression of p27Kipl and induction of cellular hypertrophy in renal tubular cells depend on the generation of oxygen radicals. Kidney Int, 1998, 54(6): 1923-1933.
1. Kajander EO. Nanobacteria-propagating calcifying nanoparticles[J]. Lett Appl Microbiol, 2006, 42(6): 549-552.
2. Ciftcioglu N, Kajander EO. Interaction of nanobacteria with cultured mammalian cells [J]. Pathophysiology, 1998, 4 (3): 259-270.
3.郑永波,吴承堂,黄祥成.纳米细菌研究进展[J].中华微生物学和免疫学杂志, 2003, 23(11): 914-915.
4. Drancourt M, Jacomo V, Lechevallier E, et al. Attempted isolation of nanobacterium sp. microorganisms from upper urinary tract stones [J]. J Clin Microbiology, 2003, 41(1): 368-372.
5. Kajander EO, Ciftcioglu N. Nanobacteria: An alternative mechanism for pathogenic intra-and extracellular calcification and stone formation. Proc Natl Acad Sci USA, 1998, 95(14): 8274-8279.
6. Ciftcioglu N, Bjorklund M, Kuorikoski K, et al. Nanobacteria: an infectious cause for kidney stone formation [J]. Kidney Int, 1999, 56 (5): 1893-1898.
7. Cuerpo EG, Kajander EO, Ciftcioglu N, et al. Nanobacteria:an experimental neo-lithogenesis model[J]. Arch Esp Urol, 2000, 53(4): 291-303.
8. Akerman KK, Kuikka JT, Ciftcioglu N, et al. Radiolabeling and in vivo distribution of nanobacteria in rabbit [J]. Proc SPIE, 1997, 3111(5):436 - 442.
9. Shiekh FA, Khullar M, Singh SK. Lithogenesis: induction of renal calcifications by nanobacteria[J]. Urol Res, 2006, 34(1): 53-57.
10.胡卫国,王晓峰,徐涛等.纳米细菌大鼠肾结石模型初步建立及成石因素分析[J].北京大学学报(医学版), 2010, 42(4): 433-435.
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17. Kajander EO, Ciftcioglu N, Aho K, et al. Characteristics of nanobacteria and their possible role in stone formation [J]. Urol Res, 2003, 31 (2): 47-54.
18. Ciftcioglu N, Vejdani K, Lee O, et al. Association between Randall’s plaque and calcifying nanoparticles[J]. International Journal of Nanomedicine, 2008, 3(1): 105-115.
19. Young JD, Martel J, Young L, et al. Putative nanobacteria represent physiological remnants and culture by-products of normal calcium homeostasis [J]. PLoS One, 2009, 4(2): e4417.
20. Young JD, Martel J, Young D, et al. Characterization of Granulations of Calcium and Apatite in Serum as Pleomorphic Mineralo-Protein Complexes and as Precursors of Putative Nanobacteria [J]. PLoS One, 2009, 4(5): e5421.
2. Kajander EO. Nanobacteria-propagating calcifying nanoparticles[J]. Lett Appl Microbiol, 2006, 42(6): 549-552.
3. Hjelle JT, Miller-Hjelle MA, Poxton IR. Endotoxin and nanobactera in polycystic kidney disease[J]. Kidney Int, 2000, 57(6): 2360-2374.
4. Sommer A, Oron U, Pretorius AM, et al. A preliminary investigation into light- modulated replication of nanobacteria and heart disease [J]. J Clin Laser Med & Surg, 2003, 21(4): 23l-235.
5. Puskas LG, Tiszlavicz L. Detection of nanobacteria like particles in human atherosclerotic plaques [J]. Acta Biol Hung, 2005, 56(3～4): 233-245.
6. WEN Yu, LI Yongguo, YANG Zhulin, et al. Nanobacteria in serum, bile and gallbladder mucosa of cholecystolithiasis patients [J]. Zhonghua Wai Ke Za Zhi, 2003, 4l(4): 267-270.
7. Turgut Demir. Is there any relation of nanobacteria with periodontal diseases [J]? Medical Hypotheses, 2008, 70, 36-39.
8. ZHOU Zhansong, LI Hong, SHEN Xuecheng, et al. Detection of nanobacteria infection in typeШprostatitis [J]. Urology, 2008, 71(6): 1091-1095.
9.唐中华,吴唯,吕新生,等.乳腺癌组织中钙化性纳米微粒样颗粒的电镜观察[J].医学临床研究, 2002, 19(3): 214-215.
10.王学军,杨竹林,文宇,等.慢性肝病、原发性肝癌病人血清、肝组织钙化性纳米微粒的检测[J].中华肝胆外科杂志, 2006, 12(3): 193-196.
11. Hudelist G, Singer CF, Kubista E, et al. Presence of nanobacteria in psammoma bodies of ovarian cancer: evidence for pathogenetic role in intratumoral biomineralization [J]. Histopathology, 2004, 45(6): 633-637.
12. Ciftcioglu N, Kajander EO. Interaction of nanobacteria with cultured mammalian cells [J]. Pathophysiology, 1998, 4 (3): 259-270.
13. Coe FL, Evan A, Worcester E. Kidney stone disease. J Clin Invest. 2005, 115(10): 2598-2608.
14. Liang L, Chen J, Vittal R, et al. Expression profiling of crystal-induced injury in human kidney epithelial cells. Nephron Physiol. 2006, 103(1): 53-62.
15. Akerman KK, Kuikka JT, Ciftcioglu N, et al. Radiolabeling and in vivo distribution of nanobacteria in rabbit [J]. Proc SPIE, 1997, 3111(5):436 - 442.
16. Cuerpo EG, Kajander EO, Ciftcioglu N, et al. Nanobacteria:an experimental neo-lithogenesis model[J]. Arch Esp Urol, 2000, 53(4): 291-303.
17. Shiekh FA, Khullar M, Singh SK. Lithogenesis: induction of renal calcifications by nanobacteria[J]. Urol Res, 2006, 34(1): 53-57.
18. Kajander EO, Ciftcioglu N. Nanobacteria: an alternative mechanism for pathogenic intra-and extracellular calcification and stone formation. Proc Natl Acad Sci USA, 1998, 95(14): 8274-8279.
19. Kajander EO, Ciftcioglu N, Aho K, et al. Characteristics of nanobacteria and their possible role in stone formation [J]. Urol Res, 2003, 31 (2): 47-54.
20.陶芝伟,邓耀良,黎承杨.利用电镜技术对尿路钙化性纳米微粒的初步观察[J].广西医科大学学报, 2009, 26(6): 837-839.
21. Young JD, Martel J, Young L, et al. Putative nanobacteria represent physiological remnants and culture by-products of normal calcium homeostasis [J]. PLoS One, 2009, 4(2): e4417.
22. Young JD, Martel J, Young D, et al. Characterization of granulations of calcium and apatite in serum as pleomorphic mineralo-protein complexes and as precursors of putative nanobacteria [J]. PLoS One, 2009, 4(5): e5421.
23. Saldeen J. Cytokines induce both necrosis and apoptosis via a common Bcl-2 inhibitable pathway in rat insulin-producing cells. Endocrinology, 2000, 141(6): 2003-2010.
24. Peart J, Willems L, Headrick JP. Receptor and non-receptor-dependent mechanisms of cardioprotection with adenosine. Am J Physiol Heart Circ Physiol, 2003, 284(2): 519-527.
25. Scheid C, Koul H, Hill WA et al. Oxalate toxicity in LLC-PK1 cells, a line ofrenal epithelial cells. J Uro1, 1996, 15 5: 1112-1116.
26. Thamilselvan S, Hackett RL, and Khan SR. Lipid peroxidation in ethylene glycol induced hyperoxaluria and calcium oxalate nephrolithiasis. J Uro1, 1997, 157: 1059-1063.
27. Khand FD, Gordge MP- Robertson WC, et al. Mitochondrial superoxide production during oxalate mediated oxidative stress in renal epithelial ce1ls.Free Radic Biol Med, 2002, 32: 1339-1350.
28. Asaba K, Tojo A, Onozato et al. Effects of NADPH oxidase inhibitor in diabetic nephropathy. Kidney Int, 2005, 67:1890-1898.
29. Engels F, Renirie BF, Hart BA,et al. Effects of apocynin, a drug isolated from the roots of Picrorhiza kurroa, on arachidonic acid metabolism. FEBS Lett, 1992, 305:254-256.
30.司徒镇强,吴军正.细胞培养.西安:世界图书出版公司,2004, 250-252.
31. Danielyan I, Mueller L, Proksch B, et al. Similar protective effects of BQ-123 and erythropoietin on survival of neural cells and generation of neurons upon hypoxic injury. Eur J Cell Biol, 2005, 84(11): 907-913
32. Carrier RL, Ma TC, Obrietan K, et al. A sensitive and selective assay of neuronal degeneration in cell culture. J Neurosci Methods, 2006, 154(1-2):239-244.
33. Huang HS, Ma MC, Chen CF, et al. Lipid peroxidation and its correlations with urinary levels of oxalate, citric acid, and ostepopontin in patients with renal calcium oxalate stones[J]. Urology, 2003, 62(6): 1123-1128.
34. Tungsange K, Sriboonlue P, Futrakul P, et al. Renal tubular cell damage and oxidative stress in renal stone patients and the effect of potassium citrate treatment[J]. Urol Res, 2005, 33(1): 65-69.
35. Carl Friedrich Verkoelen. Crystal retention in renal stone diease: a crucial role for the glycosaminoglycan hyaluronan? J Am Soc Nephrol, 2006, 17: 1673-1687.
36. Tsuiihata M. Mechanism of calcium oxalate renal atone formation and renal tubular cell injury. Int J Uml, 2008, 15: 115-120.
37. Khan SR. Renal tubular damage/dysfunction: key to the formation of kidney stones. Urol Res, 2006, 34: 86-91.
38. Crystal-induced inflammation of the kidneys, results of human, animal model and tissue culture studies. Clin Exp Nephrol, 2004, 8: 75-88.
39.关晓峰,邓耀良,黎承杨,等.巨噬细胞在高草酸尿症大鼠肾内结石晶体形成过程中的作用[J].中华泌尿外科杂志,2010,31(2):88-91.
40. Juranek I, Bezek S. Controversy of free radical hypothesis: reactive oxygen species—cause or consequence of tissue injury? Gen Physiol Biophys, 2005, 24(3):263-278.
41. Nagata M. Inflammatory cells and oxygen radicals. Curr Drug Targets Inflamm Allergy, 2005, 4(4): 503-504.
42. Victor VM, Rocha M, Esplugues JV, et al. Role of free radicals in sepsis: antioxidant therapy. Curr Pharm Des, 2005, 11(24):3141-3158.
43. 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 .Nephrology Dialysis Transplantation, 2005, 20: 870-878.
44. Rashed T, Menon M, Thamilselvan S. Molecular mechanism of oxalate-induced free radical production and glutathione redox imbalance in renal epithelial cells: effect of antioxidants. Am J Nephrol, 2004, 24: 557-568.
45. Li CY, Deng YL, Sun BH. Taurine protected kidney from oxidative injury through mitochondrial-linked pathway in a rat model of nephrolithiasis [J]. Urol Res, 2009, 37(4): 211-220.
46. Li CY, Deng YL, Sun BH. 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.
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