Three carboxymethylated Poria cocos polysaccharides (PCP‐C1, PCP‐C2, and PCP‐C3) with ‐COOH contents of 6.13%, 10.24%, and 16.22%, respectively, were obtained by carboxymethylation of the original polysaccharide (PCP‐C0), which has a molecular weight of 4 kDa and a carboxyl (‐COOH) content of 2.54%. The structure of the PCP‐Cs was characterized by FT‐IR, ¹H NMR, and ¹³C NMR spectra. The four PCP‐Cs exhibited antioxidant activity, and their ability to scavenge radicals (hydroxyl and DPPH) and chelate ferrous ions was positively correlated with the degree of carboxymethylation. As the content of ‐COOH groups in the PCP‐Cs increases, their ability to regulate the growth of calcium oxalate (CaOx) crystals was enhanced, thus inhibiting the growth of calcium oxalate monohydrate (COM) crystals and inducing the formation of more calcium oxalate dihydrate (COD) crystals. The formed CaOx crystal was more round and blunt, the absolute value of the Zeta potential on the crystal surface increased, and the aggregation between crystals was inhibited. Thermogravimetric analysis curves showed that the proportions of PCP‐C0, PCP‐C1, PCP‐C2, and PCP‐C3 incorporated into the crystal were 20.52%, 15.60%, 10.65%, and 9.78%, respectively, in the presence of 0.4 g/L PCP‐Cs. PCP‐C protection resisted oxidative damages of human kidney proximal tubular epithelial cells (HK‐2) caused by oxalate, resulting in increased cell viability and superoxide dismutase activity and decreased reactive oxygen species levels, malondialdehyde content, and 8‐hydroxy‐deoxyguanosine expression. Hence, PCP‐Cs, especially PCP‐C3, can inhibit the formation of CaOx crystals and may have the potential to be an alternative antistone drug.

Background: Kidney stone formation is closely related to renal epithelial cell damage and the adhesion of calcium oxalate crystals to cells. Methods: In this research, the adhesion of human kidney proximal tubular epithelial cells (HK-2) to calcium oxalate monohydrate crystals with a size of approximately 100 nm was studied. In addition, the inhibition of crystal adhesion by four tea polysaccharides (TPS0, TPS1, TPS2, and TPS3) with the molecular weights of 10.88, 8.16, 4.82, and 2.31 kDa, respectively were compared. Results: When oxalic acid-damaged HK-2 cells were repaired, cell viability increased. By contrast, reactive oxygen species level, phosphatidylserine eversion, and osteopontin expression decreased, thus indicating that tea polysaccharides have a repairing effect on damaged HK-2 cells. Moreover, after repairing the damaged cells, the amount of adherent crystals was reduced. The repair effect of tea polysaccharides is closely related to molecular weight, and TPS2 with the moderate molecular weight displayed the best repair effect. Conclusion: These results suggest that tea polysaccharides, especially TPS2, may inhibit the formation and recurrence of calcium oxalate kidney stones.

Neuroblastoma is the most frequently diagnosed neural tumor of childhood. Abnormal function of the long intergenic non-coding RNA (lincRNA) LINC00673 has been implicated in various human malignancies. Genome-wide association studies revealed the LINC00673 rs11655237 C>T polymorphism to be associated with the risk of neuroblastoma, though the effect was not well defined, in part due to the small sample size in our earlier study. Herein, we verified the impact of LINC00673 rs11655237 C>T on the risk of neuroblastoma in 700 cases and 1516 controls from six centers in China. After pooling all enrolled patients, we observed a significant association between LINC00673 rs11655237 C>T and risk of neuroblastoma (TT vs. CC: adjusted odds ratio [OR]=1.58, 95% confidence interval [CI]=1.06-2.35, P=0.024; additive model: adjusted OR=1.20, 95% CI=1.03-1.39, P=0.020; recessive model: adjusted OR=1.50, 95% CI=1.02-2.22, P=0.040). Stratification analysis revealed a significant relationship between rs11655237 CT/TT and neuroblastoma risk in subgroups of males, patients whose tumor originated in the adrenal gland, and patients with clinical stage IV disease. These findings add new evidence of the importance of LINC00673 rs11655237 C>T to the risk of developing neuroblastoma.

Crystal adhesion is an important link in the formation of kidney stones. This study investigated and compared the adhesion differences between nano-calcium oxalate monohydrate (COM) and human renal proximal tubule epithelial (HK-2) cells before and after treatment with tea polysaccharides (TPSs) TPS0, TPS1, TPS2, and TPS3 with molecular weights of 10.88, 8.16, 4.82, and 2.31 kDa, respectively. TPS treatment effectively reduced the damage of COM to HK-2 cells, thereby resulting in increased cell activity, decreased release of lactate dehydrogenase, cell morphology recovery, decreased level of reactive oxygen species, increased mitochondrial membrane potential, increased lysosomal integrity, decreased expression of adhesion molecule osteopontin and eversion of phosphatidylserine, and decreased crystal adhesion. Among the TPSs, TPS2 with moderate molecular weight had the best protective effect on cells and the strongest effect on the inhibition of crystal adhesion. Thus, TPS2 may be a potential anticalculus drug.

The protective effects of Porphyra yezoensis polysaccharides (PYPs) with molecular weights of 576.2 (PYP1), 105.4 (PYP2), 22.47 (PYP3), and 3.89 kDa (PYP4) on the oxidative damage of human kidney proximal tubular epithelial (HK‐2) cells and the differences in adherence and endocytosis of HK‐2 cells to calcium oxalate monohydrate crystals before and after protection were investigated. Results showed that PYPs can effectively reduce the oxidative damage of oxalic acid to HK‐2 cells. Under the preprotection of PYPs, cell viability increased, cell morphology improved, reactive oxygen species levels decreased, mitochondrial membrane potential increased, S phase cell arrest was inhibited, the cell apoptosis rate decreased, phosphatidylserine exposure reduced, the number of crystals adhered to the cell surface reduced, but the ability of cells to endocytose crystals enhanced. The lower the molecular weight, the better the protective effect of PYP. The results in this article indicated that PYPs can reduce the risk of kidney stone formation by protecting renal epithelial cells from oxidative damage and reducing calcium oxalate crystal adhesion, and PYP4 with the lowest molecular weight may be a potential drug for preventing kidney stone formation.