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.

矿化结晶被认为是石材形成的初始阶段。然而，很少研究晶体的形成和随后的细胞损伤。使用草酸建立人近端肾小管上皮细胞（HK-2）的氧化损伤的细胞模型。随后，通过添加2.0 mmol / L的草酸钠溶液诱导CaOx结晶。我们比较了分子量分别为49.54 kDa（PYP1）和4.02 kDa（PYP2）和K ₃的PYP的协同效应引用抑制CaOx结晶的方法，研究了CaOx晶体在细胞表面的成核，生长和保留过程，以及随后形成的晶体对细胞的破坏。正常的HK-2细胞主要诱导CaOx二水合物（COD）的形成，而受损细胞主要诱导CaOx一水合物（COM）晶体的形成。在PYPs的保护下，细胞状态得到改善，并且COD晶体在形成的晶体中的比例增加。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K ₃的协同作用下Cit，形成的晶体数量明显减少，并且尺寸明显减小。PYP可以修复受损细胞并抑制COD相向COM相的转化。K ₃ Cit可以明显抑制CaOx晶体的形核并减少晶体形成的数量。PYP修复受损细胞，以及PYP和K ₃ Cit对CaOx结晶的协同抑制作用可减少细胞损伤和细胞表面晶体形成。通过同时修复受损的细胞并抑制结晶，该策略有望在防止结石形成和复发方面发挥理想的作用。