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纳米细菌在肾结石形成发病机制中的作用。

Role of nanobacteria in the pathogenesis of kidney stone formation.

作者信息

Hong Xin, Wang Xiaofeng, Wang Tian, Yu Chengfan, Li Hui

机构信息

Department of Urology, Peking University International Hospital Beijing 102206, China.

出版信息

Am J Transl Res. 2016 Jul 15;8(7):3227-34. eCollection 2016.

PMID:27508044
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4969460/
Abstract

OBJECTIVE

This study aimed to investigate the nanobacteria (NB) induced damage to human tubular epithelial HK-2 cells and the potential role of NB in the kidney stone formation.

METHODS

Serum sample from 15 patients with kidney stone was collected. Four groups were included: control, NB group, nanograde hydroxyapatite (nHAP) and calcium oxalate monohydrate (COM) group. Catalase (CAT), malonaldehyde (MDA) and Na(+)/K(+) ATPase activity was detected in the supernatant at 12 and 24 h. At 12 and 24 h, COM was added.

RESULTS

At 12 h and 24 h, the CAT in NB group was significantly higher than in control group and nHAP group (P<0.01). CAT at 24 h was significantly higher than in COM group (P<0.01). At 12 h and 24 h, the MDA in NB group was significantly higher than in control group and nHAP group (P<0.01) and significantly lower than in COM group (P<0.01). At 12 h, the Na(+)/K(+) ATPase activity in NB group and nHAP group was significantly lower than in control group, but dramatically increased as compared to COM group (P<0.01). At 24 h, the Na(+)/K(+) ATPase activity in NB group and nHAP group was significantly lower than in control group (P<0.01).

CONCLUSION

NB may induce lipid peroxidation in HK-2 cells and cause adhesion of HK-2 cells to COM in a time-dependent manner, resulting in damage to HK-2 cells. This injury-causing capability of NB is more potent than nHAP and might be involved in the pathogenesis of kidney stone formation.

摘要

目的

本研究旨在探讨纳米细菌(NB)对人肾小管上皮HK - 2细胞的损伤作用以及NB在肾结石形成中的潜在作用。

方法

收集15例肾结石患者的血清样本。分为四组:对照组、NB组、纳米级羟基磷灰石(nHAP)组和一水合草酸钙(COM)组。在12小时和24小时时检测上清液中的过氧化氢酶(CAT)、丙二醛(MDA)和Na(+)/K(+) ATP酶活性。在12小时和24小时时加入COM。

结果

在12小时和24小时时,NB组的CAT显著高于对照组和nHAP组(P<0.01)。24小时时的CAT显著高于COM组(P<0.01)。在12小时和24小时时,NB组的MDA显著高于对照组和nHAP组(P<0.01),且显著低于COM组(P<0.01)。在12小时时,NB组和nHAP组的Na(+)/K(+) ATP酶活性显著低于对照组,但与COM组相比显著升高(P<0.01)。在24小时时,NB组和nHAP组的Na(+)/K(+) ATP酶活性显著低于对照组(P<0.01)。

结论

NB可能诱导HK - 2细胞发生脂质过氧化,并以时间依赖性方式导致HK - 2细胞与COM黏附,从而对HK - 2细胞造成损伤。NB的这种致伤能力比nHAP更强,可能参与了肾结石形成的发病机制。

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Kidney Int. 2005 Aug;68(2):497-503. doi: 10.1111/j.1523-1755.2005.00427.x.
2
A potential cause for kidney stone formation during space flights: enhanced growth of nanobacteria in microgravity.太空飞行期间肾结石形成的一个潜在原因:微重力环境下纳米细菌的生长增强。
Kidney Int. 2005 Feb;67(2):483-91. doi: 10.1111/j.1523-1755.2005.67105.x.
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The effect of ions at the surface of calcium oxalate monohydrate crystals on cell-crystal interactions.一水合草酸钙晶体表面离子对细胞 - 晶体相互作用的影响。
Urol Res. 2004 May;32(2):117-23. doi: 10.1007/s00240-003-0391-5. Epub 2003 Dec 9.
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Calcium oxalate crystal adherence to hyaluronan-, osteopontin-, and CD44-expressing injured/regenerating tubular epithelial cells in rat kidneys.草酸钙晶体与大鼠肾脏中表达透明质酸、骨桥蛋白和CD44的损伤/再生肾小管上皮细胞的黏附。
J Am Soc Nephrol. 2003 Dec;14(12):3155-66. doi: 10.1097/01.asn.0000099380.18995.f7.
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Nephron Exp Nephrol. 2003;94(3):e103-12. doi: 10.1159/000072028.
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Curr Pharm Des. 2003;9(12):975-81. doi: 10.2174/1381612033455125.
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Urol Res. 2003 Jun;31(2):47-54. doi: 10.1007/s00240-003-0304-7. Epub 2003 Mar 27.
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Adhesion between molecules and calcium oxalate crystals: critical interactions in kidney stone formation.分子与草酸钙晶体之间的粘附:肾结石形成中的关键相互作用。
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COM crystals activate the p38 mitogen-activated protein kinase signal transduction pathway in renal epithelial cells.COM晶体激活肾上皮细胞中的p38丝裂原活化蛋白激酶信号转导通路。
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