Metabolomic study of serum from rabbits with acute acalculous cholecystitis
Objectives 1 H-NMR is a powerful approach of metabolomics. This study aimed to apply it to detect the serum metabolites in rabbits with acute acalculous cholecystitis (AAC), and to analyze their potential roles in AAC. Methods Fourteen rabbits were randomly divided into two groups, the AAC group and...
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Veröffentlicht in: | Inflammation research 2012-09, Vol.61 (9), p.987-995 |
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Sprache: | eng |
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Zusammenfassung: | Objectives
1
H-NMR is a powerful approach of metabolomics. This study aimed to apply it to detect the serum metabolites in rabbits with acute acalculous cholecystitis (AAC), and to analyze their potential roles in AAC.
Methods
Fourteen rabbits were randomly divided into two groups, the AAC group and the CON group. In the AAC rabbit model,
Escherichia coli
solution was injected into the gallbladder, while same volume of saline, instead of
E. coli
solution, was injected into the gallbladder of the CON rabbit. General morphological, light microscopic and transmission electron microscopic observations were used to evaluate the model. Metabolic profiles of serum from rabbits with AAC were investigated through
1
H-NMR spectroscopy coupled with multivariate statistical analysis, such as principal components analysis and orthogonal partial least-squares discriminant analysis.
Results
The pathohistology of gallbladders showed a significant difference between the two groups, proving the successful induction of inflammation in the gallbladders of the AAC group. The serum concentration of lipids (LDL and VLDL) increased during AAC, while the concentrations of phospholipids, lactic acid, 3-hydroxybutyric acid, lysine, citric acid, asparagine, histidine, glucose and some other small molecular metabolites decreased.
Conclusion
The profiling of serum metabolites in rabbits with acute acalculous cholecystitis changed significantly. These changes referred to the metabolic disturbance of carbohydrate, amino acids and lipids, inhibition of immunological functions and inflammation reaction. |
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ISSN: | 1023-3830 1420-908X |
DOI: | 10.1007/s00011-012-0491-1 |