An ultra performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry (UPLC Q-TOF MS) metabonomics approach was employed to study the serum metabolic profiling of adenine-induced chronic renal failure (CRF) rats. Acquired data were subjected to principal component analysis (PCA) for differentiating the CRF and the normal control groups. Potential biomarkers were screened by using S-plot and were identified by the accurate mass, isotopic pattern and MS/MS fragments information obtained from UPLC Q-TOF MS analysis. Significant differences in the serum level of creatinine, amino acids and LysoPCs were observed, indicating the perturbations of amino acid metabolism and phospholipid metabolism in adenine-induced CRF rats. This research proved that metabonomics is a promising tool for disease research.

Download full-text PDF

Source
http://dx.doi.org/10.3109/1354750X.2011.637180DOI Listing

Publication Analysis

Top Keywords

adenine-induced chronic
8
chronic renal
8
renal failure
8
ultra performance
8
performance liquid
8
liquid chromatography
8
chromatography coupled
8
coupled quadrupole
8
quadrupole time-of-flight
8
time-of-flight mass
8

Similar Publications

Sinomenine attenuates uremia vascular calcification by miR-143-5p.

Sci Rep

January 2025

Department of Nephrology, Yiyang Central Hospital, 118 Kangfubei Road, Yiyang, 413000, Hunan, China.

Vascular calcification is considered to be a killer of the cardiovascular system, involved inflammation and immunity. There is no approved therapeutic strategy for the prevention of vascular calcification. Sinomenine exhibited anti-inflammatory and immunosuppressive effects.

View Article and Find Full Text PDF

Patients with chronic inflammation are burdened with anemia of inflammation (AI), where inflammatory cytokines inhibit erythropoiesis, impede erythropoietin production, and limit iron availability by inducing the iron regulator hepcidin. High hepcidin hinders iron absorption and recycling, thereby worsening the impaired erythropoiesis by restricting iron availability. AI management is important as anemia impacts quality of life and potentially affects morbidity and mortality.

View Article and Find Full Text PDF

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 PDF

Runx2-NLRP3 Axis Orchestrates Matrix Stiffness-evoked Vascular Smooth Muscle Cell Inflammation.

Am J Physiol Cell Physiol

January 2025

Department of Physiology and Pathophysiology, School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China.

Arterial stiffening is a hallmark of chronic kidney disease (CKD) related cardiovascular events and is primarily attributed to the elevated matrix stiffness. Stiffened arteries are accompanied by low-grade inflammation, but the causal effects of matrix stiffness on inflammation remain unknown. For analysis of the relationship between arterial stiffness and vascular inflammation, pulse wave velocity (PWV) and aortic inflammatory markers were analyzed in an adenine-induced mouse model of CKD in chronological order.

View Article and Find Full Text PDF

Glycerol-3-phosphate contributes to the increase in FGF23 production in chronic kidney disease.

Am 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.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!