Department of Urology, the Affiliated Children's Hospital of Xiangya School of Medicine, Central South University (Hunan Children's Hospital), Changsha, China.
Institute of Biomineralization and Lithiasis Research, College of Chemistry and Materials Science, Jinan University, Guangzhou, China.
J Cell Physiol. 2024 Jun;239(6):e31272. doi: 10.1002/jcp.31272. Epub 2024 Apr 22.
The inhibition of cell surface crystal adhesion and an appropriate increase in crystal endocytosis contribute to the inhibition of kidney stone formation. In this study, we investigated the effects of different degrees of carboxymethylation on these processes. An injury model was established by treating human renal proximal tubular epithelial (HK-2) cells with 98.3 ± 8.1 nm calcium oxalate dihydrate (nanoCOD) crystals. The HK-2 cells were protected with carboxy (-COOH) Desmodium styracifolium polysaccharides at 1.17% (DSP0), 7.45% (CDSP1), 12.2% (CDSP2), and 17.7% (CDSP3). Changes in biochemical indexes and effects on nanoCOD adhesion and endocytosis were detected. The protection of HK-2 cells from nanoCOD-induced oxidative damage by carboxymethylated Desmodium styracifolium polysaccharides (CDSPs) is closely related to the protection of subcellular organelles, such as mitochondria. CDSPs can reduce crystal adhesion on the cell surface and maintain appropriate crystal endocytosis, thereby reducing the risk of kidney stone formation. CDSP2 with moderate -COOH content showed the strongest protective activity among the CDSPs.
抑制细胞表面晶体黏附，适当增加晶体内吞作用有助于抑制肾结石形成。本研究探讨了不同羧甲基化程度对这些过程的影响。通过用 98.3±8.1nm 草酸钙二水合物（nanoCOD）晶体处理人肾近端肾小管上皮（HK-2）细胞，建立损伤模型。用 1.17%（DSP0）、7.45%（CDSP1）、12.2%（CDSP2）和 17.7%（CDSP3）羧甲基（-COOH）舞草多糖（CDSPs）保护 HK-2 细胞。检测生化指标的变化及对 nanoCOD 黏附和内吞作用的影响。羧甲基化舞草多糖（CDSPs）对 HK-2 细胞免受 nanoCOD 诱导的氧化损伤的保护作用与对线粒体等亚细胞细胞器的保护密切相关。CDSPs 可减少细胞表面晶体黏附，并维持适当的晶体内吞作用，从而降低肾结石形成的风险。羧基含量适中的 CDSP2 在 CDSPs 中表现出最强的保护活性。
