Aim: Cerium oxide, particularly in nanoparticle form (nanoceria), has been investigated for biomedical applications as a promising new agent for treating several pathologies. The aim of the present study was to characterize the pharmacologic effects of nanoceria in an animal model of chronic kidney disease.
Methods: We created the chronic kidney disease animal model by feeding rats a 0.25% adenine diet. Male Wistar rats were divided into five groups: normal diet, 0.25% adenine diet, or adenine diet containing three different doses or durations of nanoceria treatment. Blood was collected weekly from the tail veins of each rat and analyzed for renal function markers. After 5 weeks, various biochemical markers in serum, plasma, and urine were also analyzed.
Results: In the adenine-treated group, body weight was significantly decreased, and the kidneys lost much of their healthy reddish color and became lumpy and white in appearance. In addition, levels of serum creatinine, blood urea nitrogen, and plasma uremic toxins were significantly increased in adenine-treated rats compared with controls. Renal functional and structural damage in adenine diet model rats tended to be ameliorated by nanoceria ingestion. The high-dose cerium-treated group maintained reddish areas in the kidneys, and the increases in biomarker levels of creatinine, blood urea nitrogen, and inorganic phosphorus were markedly reduced, regardless of treatment duration.
Conclusions: Ingestion of nanoceria may be effective for improving or preventing renal damage caused by adenine. Geriatr Gerontol Int 2024; 24: 88-95.
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http://dx.doi.org/10.1111/ggi.14739 | DOI Listing |
Theranostics
January 2025
Department of Nephrology, Jiangsu Province Hospital, The First Affiliated Hospital of Nanjing Medical University, Nanjing Medical University, 300 Guangzhou Road, Nanjing 210029, China.
Chronic kidney disease (CKD) is a global public health issue, with vascular calcification (VC) being a common and deadly complication. Despite its prevalence, the underlying mechanisms of VC remain unclear. In this study, we aimed to investigate whether and how Otubain-2 (OTUB2) contributes to VC.
View Article and Find Full Text PDFCells
December 2024
Department of Medicine, College of Medicine and Life Sciences, University of Toledo, Toledo, OH 43614, USA.
Commonly used adenine-induced chronic kidney disease (CKD) murine models often employ C57BL/6 mice; however, this strain has inherent limitations due to its natural resistance to developing key pathological features of CKD, such as tubulointerstitial fibrosis and inflammation. There have been attempts to overcome these barriers by using multiple concentrations of adenine-supplemented diets or by performing prolonged experiments up to 20 weeks. Here, we demonstrate that SKH1 Elite mice develop clinically relevant CKD phenotypes (e.
View Article and Find Full Text PDFAntioxidants (Basel)
December 2024
Polymeric Biomaterials Laboratory, Department of Materials and Optoelectronic Science, National Sun Yat-Sen University, Kaohsiung 804, Taiwan.
Sodium thiosulfate (STS), a precursor of hydrogen sulfide (HS), has demonstrated antihypertensive properties. Previous studies have suggested that HS-based interventions can prevent hypertension in pediatric chronic kidney disease (CKD). However, the clinical application of STS is limited by its rapid release and intravenous administration.
View Article and Find Full Text PDFBiosens Bioelectron
March 2025
Department of Cogno-Mechatronics Engineering, College of Nanoscience and Nanotechnology, Pusan National University, Busan, 46241, Republic of Korea. Electronic address:
Creatinine (Ctn) is a biomarker for chronic kidney disease (CKD). In this study, a highly sensitive and specific detection method for Ctn based on a molecularly imprinted polymer (MIP) based electrochemical biosensor was developed. Mxene (Mx), which has high absorption properties, was modified using carbon screen-printed electrodes (SPCE).
View Article and Find Full Text PDFAm J Physiol Renal Physiol
December 2024
Nephrology Division, Department of Medicine, Massachusetts General Hospital, Boston, MA , USAXXXX, XXX.
Why fibroblast growth factor 23 (FGF23) levels increase markedly in chronic kidney disease (CKD) is unknown. Recently, we found that phosphate stimulates renal production of glycerol-3-phosphate (G-3-P), which circulates to bone to trigger FGF23 production. To assess the impact of G-3-P on FGF23 production in CKD, we compared the effect of adenine-induced CKD in mice deficient in glycerol-3-phosphate dehydrogenase 1 (Gpd1), an enzyme that synthesizes G-3-P, along with wild-type littermates.
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