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Concentration-dependent Cellular Injuries Induced by Calcium Oxalate Monohydrate and Dihydrate Crystals

机译:草酸钙一水合物和二水合物晶体诱导浓度依赖性细胞损伤

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This study aims to compare the cytotoxicity and adhesion of calcium oxalate monohydrate (COM) and dehydrate (COD) crystals with a size of 5 μm toward human kidney proximal tubular epithelial (HKC) cells so as to reveal the mechanism of kidney stone formation at cellular level. The measurement of cell viability and Lactate dehydrogenase (LDH) content were used to quantitatively analyze cell injury induced by COM and COD crystals; cell mortality was measured by propidium iodide (PI) staining; the adhesion of crystals on cell surface was observed by SEM. The decrease of cell viability and increase of LDH release of HKC cells caused by COM and COD were concentration-dependent in crystal concentration range of 100~1600 μg/mL. COM caused more serious injury in HKC than COD. The adhesion amount of COM was significantly greater than COD crystal. The damage of micron COM was larger than COD, and COM was more easily aggregated on HKC. The results in this paper indicated that the presence of COM crystals in urine was more likely to increase the risk of stone formation than COD crystals.
机译:本研究旨在将草酸钙单水合物(COM)和脱水(COD)晶体的细胞毒性和粘附性与朝向人肾近端管状上皮(HKC)细胞的尺寸进行比较,以揭示细胞肾结石形成的机制等级。用于定量分析COM和COD晶体诱导的细胞损伤的细胞活力和乳酸脱氢酶(LDH)含量的测量;通过碘化丙啶(PI)染色来测量细胞死亡率;通过SEM观察晶体对细胞表面上的粘附性。由COM和COD引起的COM和COM引起的HKC细胞的LDH释放的降低浓度依赖于100〜1600μg/ mL的晶体浓度范围。 COM引起了比COD的更严重的伤害。 COM的粘合量明显大于COD晶体。微米COM的损坏大于COD,并且在HKC上更容易聚集COM。本文的结果表明,尿液中的COM晶体的存在更可能增加石形成的风险而不是COD晶体。

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