Porphyra yezoensis polysaccharide and potassium citrate synergistically inhibit calcium oxalate crystallization induced by renal epithelial cells and cytotoxicity of the formed crystals.

Porphyra yezoensis polysaccharide and potassium citrate synergistically inhibit calcium oxalate crystallization induced by renal epithelial cells and cytotoxicity of the formed crystals.
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条斑紫菜多糖和柠檬酸钾协同抑制肾上皮细胞诱导的草酸钙结晶以及所形成晶体的细胞毒性。

DOI:
10.1016/j.msec.2020.111448
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发表时间:
2021-02
期刊:
Materials Science and Engineering: C
影响因子:
--
通讯作者:
Ouyang Jian-Ming
Ouyang Jian-Ming
中科院分区:
其他
文献类型:
--
作者:
Sun Xin-Yuan;Zhang Hui;Chen Jia-Yun;Zeng Guo-Hua;Ouyang Jian-Ming

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成矿结晶被认为是成石的初始阶段。然而,晶体的形成和随后的细胞损伤很少被研究。用草酸损伤人近端肾小管上皮细胞(HK-2),建立氧化损伤细胞模型。随后,加入2.0g/L的L草酸钠溶液诱导CaO_x结晶。我们比较了相对分子质量为49.54 kDa(PYP1)和4.02 kDa(PYP2)的PYPs与K3Cit对CaOx结晶的协同抑制作用,并研究了CaOx晶体在细胞表面的成核、生长和滞留过程以及形成的晶体对细胞的损伤。正常HK-2细胞主要诱导二水氧化钙(COD)的形成,而损伤细胞主要诱导一水氧化钙(COM)晶体的形成。在PYPS的保护下,细胞的状态得到改善,COD晶体在形成的晶体中所占的比例增加。与PYP1相比,小分子量PYP2具有更好的抑制CaOx结晶和改善细胞状态的能力。在PYPS和K3Cit的协同作用下,形成的晶体数量明显减少,尺寸明显减小。PYPS可修复受损细胞,并抑制COD相向COM相的转化。K3Cit能明显抑制CaOx晶体的形核,减少晶体形成量。PYPS对受损细胞的修复以及PYPS和K3Cit对CaOx结晶的协同抑制减少了细胞损伤和细胞表面晶体的形成。通过同时修复受损细胞和抑制结晶,这一策略有望在预防结石的形成和复发方面发挥理想的效果。
Mineralization crystallization is considered to be the initial stage of stone formation. However, the formation of crystals and subsequent cell damage have rarely been investigated. An oxidatively damaged cell model was established using oxalic acid to injure human proximal tubular epithelial cells (HK-2). Subsequently, CaOx crystallization was induced by adding 2.0 mmol/L sodium oxalate solution. We compared the synergistic effects of PYPs with molecular weights of 49.54 kDa (PYP1) and 4.02 kDa (PYP2) and K3Cit on the inhibition of CaOx crystallization and studied the nucleation, growth, and retention process of CaOx crystals on the cell surface and the subsequent damage of the formed crystals to the cells. Normal HK-2 cells mainly induced the formation of CaOx dihydrate (COD), whereas the damaged cells mainly induced the formation of CaOx monohydrate (COM) crystals. Under the protection of PYPs, the state of cells was improved, and the proportion of COD crystals in the formed crystals increased. Small-molecular-weight PYP2 exhibited better abilities of inhibiting CaOx crystallization and improving cell state compared with PYP1. Under the synergistic effects of PYPs and K3Cit, the number of formed crystals was obviously reduced, and the size was obviously decreased. PYPs can repair damaged cells and inhibit the conversion of COD phase to COM phase. K3Cit can obviously inhibit the nucleation of CaOx crystal and reduce the amount of crystal formation. The repair of damaged cells by PYPs and the synergistic inhibition of CaOx crystallization by PYPs and K3Cit reduce cell damage and crystal formation on the cell surface. By simultaneously repairing damaged cells and inhibiting crystallization, this strategy is expected to exert a desirable effect in preventing the formation and recurrence of stones.
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