Regulation on Calcium Oxalate Crystallization and Protection on HK-2 Cells of Tea Polysaccharides with Different Molecular Weights

Liu, Hong; Sun, Xin-Yuan; Wang, Fengxin; Ouyang, Jing

doi:10.1155/2020/5057123

Cited by 18 publications

(14 citation statements)

References 38 publications

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“…The diffraction peaks at crystal plane spacing d = 0.593, 0.364, 0.296, and 0.235 nm belong to the

, (020),

, and (130) crystal planes of calcium oxalate monohydrate (COM), respectively. The peaks at d = 0.617, 0.441, 0.277, and 0.224 nm belong to the diffraction peaks of (200), (211), (411), and (213) crystal planes of calcium oxalate dihydrate (COD), respectively [ 41 ].…”

Section: Resultsmentioning

confidence: 99%

“…In particular, ν as (COO − ) gradually shifts from 1624 cm −1 to 1644 cm −1 and ν s (COO − ) gradually shifts from 1320 cm −1 to 1329 cm −1 , indicating that the COM percentage in the CaOx crystal continuously decreases, while the COD percentage gradually increases. Given that the ν as (COO − ) and ν s (COO − ) of COD are 1644 and 1329 cm −1 [ 41 , 43 ], respectively, the blue shift values of ν as (COO − ) and ν s (COO − ) depend on the percentage of COD in the mixture.…”

Section: Resultsmentioning

confidence: 99%

“…(e, f) 13 C NMR spectra of PCP-C0 and PCP-C1.6Oxidative Medicine and Cellular Longevity monohydrate (COM), respectively. The peaks at d = 0:617, 0.441, 0.277, and 0.224 nm belong to the diffraction peaks of ð200Þ, ð211Þ, ð411Þ, and ð213Þ crystal planes of calcium oxalate dihydrate (COD), respectively[41].…”

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confidence: 99%

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Inhibition of Calcium Oxalate Formation and Antioxidant Activity of Carboxymethylated Poria cocos Polysaccharides

Liu

Zhao

et al. 2021

Oxidative Medicine and Cellular Longevity

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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.

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“…The diffraction peaks at crystal plane spacing d = 0.593, 0.364, 0.296, and 0.235 nm belong to the

, (020),

Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

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Inhibition of Calcium Oxalate Formation and Antioxidant Activity of Carboxymethylated Poria cocos Polysaccharides

Liu

Zhao

et al. 2021

Oxidative Medicine and Cellular Longevity

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“…High oxalate concentrations have been shown to increase the production of reactive oxygen species in renal tubular epithelial cells, leading to endothelial injury and apoptosis, which plays an important role in the formation of kidney crystals [14,30]. Previous studies found that oxalate treatment increased the levels of LDH, H 2 O 2 , MDA, and ROS in HK-2 cells, which indicated the activation of oxidative stress [31][32][33]. Consistent with the findings of urolithiasis studies, we found that oxidative stress was activated in uremic atherosclerotic mice with hyperoxalemia as well.…”

Section: Discussionmentioning

confidence: 97%

Hyperoxalemia Leads to Oxidative Stress in Endothelial Cells and Mice with Chronic Kidney Disease

Sun

Tang

Song

et al. 2021

Kidney Blood Press Res

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Introduction: Cardiovascular disease is the most common cause of morbidity and mortality in patients with ESRD. In addition to phosphate overload, oxalate, a common uremic toxin, is also involved in vascular calcification in patients with ESRD. The present study investigated the role and mechanism of hyperoxalemia in vascular calcification in mice with uremia. Methods: A uremic atherosclerosis (UA) model was established by left renal excision and right renal electrocoagulation in apoE−/− mice to investigate the relationship between oxalate loading and vascular calcification. After 12 weeks, serum and vascular levels of oxalate, vascular calcification, inflammatory factors (TNF-α and IL-6), oxidative stress markers (malondialdehyde [MDA], and advanced oxidation protein products [AOPP]) were assessed in UA mice. The oral oxalate-degrading microbe Oxalobacter formigenes (O. formigenes) was used to evaluate the effect of a reduction in oxalate levels on vascular calcification. The mechanism underlying the effect of oxalate loading on vascular calcification was assessed in cultured human aortic endothelial cells (HAECs) and human aortic smooth muscle cells (HASMCs). Results: Serum oxalate levels were significantly increased in UA mice. Compared to the control mice, UA mice developed more areas of aortic calcification and showed significant increases in aortic oxalate levels and serum levels of oxidative stress markers and inflammatory factors. The correlation analysis showed that serum oxalate levels were positively correlated with the vascular oxalate levels and serum MDA, AOPP, and TNF-α levels, and negatively correlated with superoxide dismutase activity. The O. formigenes intervention decreased serum and vascular oxalate levels, while did not improve vascular calcification significantly. In addition, systemic inflammation and oxidative stress were also improved in the O. formigenes group. In vitro, high concentrations of oxalate dose-dependently increased oxidative stress and inflammatory factor expression in HAECs, but not in HASMCs. Conclusions: Our results indicated that hyperoxalemia led to the systemic inflammation and the activation of oxidative stress. The reduction in oxalate levels by O. formigenes might be a promising treatment for the prevention of oxalate deposition in calcified areas of patients with ESRD.

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“…Zhao et al [11] showed that tea polysaccharides (TPS0, TPS1, TPS2, and TPS3) with Mws of 10.88, 8.16, 4.82, and 2.3 kDa, respectively, could inhibit the adhesion of calcium oxalate monohydrate (COM) to human renal proximal tubular (HK-2) cells, and TPS2 with moderate Mw had the best protective effect. In addition, TPS with lower molecular weight have a better ability to increase the percentage of the dihydrate crystalline phase in CaOx crystals and reduce the size of CaOx monohydrate crystals [12].…”

Section: Introductionmentioning

confidence: 99%

Protective Effect of Degraded Porphyra yezoensis Polysaccharides on the Oxidative Damage of Renal Epithelial Cells and on the Adhesion and Endocytosis of Nanocalcium Oxalate Crystals

Peng

Zhao

et al. 2021

Oxidative Medicine and Cellular Longevity

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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.

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Regulation on Calcium Oxalate Crystallization and Protection on HK-2 Cells of Tea Polysaccharides with Different Molecular Weights

Cited by 18 publications

References 38 publications

Inhibition of Calcium Oxalate Formation and Antioxidant Activity of Carboxymethylated Poria cocos Polysaccharides

Inhibition of Calcium Oxalate Formation and Antioxidant Activity of Carboxymethylated Poria cocos Polysaccharides

Hyperoxalemia Leads to Oxidative Stress in Endothelial Cells and Mice with Chronic Kidney Disease

Protective Effect of Degraded Porphyra yezoensis Polysaccharides on the Oxidative Damage of Renal Epithelial Cells and on the Adhesion and Endocytosis of Nanocalcium Oxalate Crystals

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