Cerium oxide-based nanozyme suppresses kidney calcium oxalate crystal depositions via reversing hyperoxaluria-induced oxidative stress damage

Abstract

Oxidative stress damage to renal epithelial cells is the main pathological factor of calcium oxalate calculi formation. The development of medicine that could alleviate oxidative damage has become the key to the prevention and treatment of urolithiasis. Herein, porous nanorods CeO2 nanoparticles (CNPs) were selected from CeO2 with different morphologies as an antioxidant reagent to suppress kidney calcium oxalate crystal depositions with excellent oxidation resistance due to its larger specific surface area. The reversible transformation from Ce3+ to Ce4+ could catalyze the decomposition of excess free radicals and act as a biological antioxidant enzyme basing on its strong ability to scavenge free radicals. The protection capability of CNPS against oxalate-induced damage and the effect of CNPS on calcium oxalate crystallization were studied. CNPS could effectively reduce reactive oxygen species production, restore mitochondrial membrane potential polarity, recover cell cycle progression, reduce cell death, and inhibit the formation of calcium oxalate crystals on the cell surface in vitro. The results of high-throughput sequencing of mRNA showed that CNPs could protect renal epithelial cells from oxidative stress damage caused by high oxalate by suppressing the expression gene of cell surface adhesion proteins. In addition, CNPS can significantly reduce the pathological damage of renal tubules and inhibit the deposition of calcium oxalate crystals in rat kidneys while having no significant side effect on other organs and physiological indicators in vivo. Our results provide a new strategy for CNPS as a potential for clinical prevention of crystalline kidney injury and crystal deposition.

Ferrous Selenide Stabilized Black Phosphorus Heterojunction Sonosensitizer for MR Imaging-Guided Sonodynamic Therapy of Bladder Cancer

“…Calcein /PI staining: MB49 cells (4 × 10 4 cells per well, 48-well plates) were treated with FeSe 2 , BP, and BFeSe 2 with the same concentration, and incubated for 8 h. The US groups were exposed to US irradiation (1.5 W/cm 2 , 3 min) and incubated for another 1 h. The calcein AM/PI detection working solution was used to stain the cells. After 30 min, the cells were observed under the fluorescence microscope [ 35 ].…”

“…Then, the cells were dispersed into 80% methanol, treated with liquid nitrogen for 15 min, and stored at −80 °C. Finally, the Vanquish UHPLC system (Thermo Fisher) was used to perform ultra-high-performance liquid chromatography–mass spectrometry analysis on the cells [ 34 ].…”

Revitalizing Ancient Mitochondria with Nano‐Strategies: Mitochondria‐Remedying Nanodrugs Concentrate on Disease Control

“…CNPs [ 299] --≈50nm (length) -CeO 2 I/R-or UUO-induced renal injury IL-10@PLT [300] --965-3254 -IL-10…”

A comprehensive study of oxidative stress‐related effects on the prognosis and drug therapy of cervical cancer

“…13 The high levels of reactive oxygen species (ROS) during OS can lead to the impairment of macromolecules such as proteins, lipids and nucleic acids when cells resist apoptosis or undergo aging. [14][15][16][17] Maintaining the integrity of DNA or RNA, proteins and lipids is crucial for overall health and disease prevention. Prior research has highlighted the significant role of OS in various human diseases, including cancer.…”

“…OS can lead to cell senescence and apoptosis, 11,12 which serve as defense mechanisms to limit the growth of damaged cells, thereby preventing the propagation of genetic instability and damage to progeny cells 13 . The high levels of reactive oxygen species (ROS) during OS can lead to the impairment of macromolecules such as proteins, lipids and nucleic acids when cells resist apoptosis or undergo aging 14–17 . Maintaining the integrity of DNA or RNA, proteins and lipids is crucial for overall health and disease prevention.…”