Al-known standards and artificial Rivaroxaban Factor Xa inhibitor peaks, such as Ger Uschspitzen caused by S And BSTFA derivatization procedure ulenbluten were removed from the dataset. The UPLC-TOF MS and ES ES The raw data were analyzed by MarkerLynx Applications Manager version 4.1. A list of intensity Th of each ion peak detected was produced, with the retention times and pairs m / z data identifier for each ion. The resulting three-dimensional matrix containing randomly assigned indexes advanced, the names of the sample, and the ionic Strength information. For koh Pension derived Gr S was reduced, the resulting matrix further by removing the tips with the missing value in more than 30% of the samples from two model and control groups. The peaks of ions generated by the internal standard were also removed. Independent Independent t-test was used to with p = 0.01 for the difference between the controlled variables And the model groups and 0.05 percent between the model and fosinopril treatment group to compare each. The corresponding Fold change was calculated for each variable, in order to show how they vary between controlled And the model groups / fosinopril. Pearson correlation between the metabolites analyzed and biochemical / pathological values of parameters were performed by SPSS 15.0. The identification of compounds was determined by GC-TOF-MS analysis by comparison with NIST fragments Mass spectral database 08 flat in NIST MS Search 2.0 software with a Performed similarity of more than 70%, and conclude checked Lich by compounds determined reference . Identification of metabolites differentials UPLC TOFMS was accurate with a total molecular weight, ES and ES You cross fashion to facilitate analysis, collision induced dissociation of the source technology, pattern matching and without isotope database online. Three for Premix toxin molecules have been validated using commercial materials. Results and discussion 3.1
. Animal model of diabetic kidney disease and the therapeutic effects of ACE inhibitors on kidney damage Ending, as in Figures 1 and 2, after administration of STZ nephrotectomy and right, all rats developed hyperglycemia Chemistry and diabetic kidney damage To, including normal massive proteinuria , the expansion of the mesangial matrix, glomerulosclerosis, cast iron protein, expansion or Tubul re atrophy and infiltration of inflammatory cells, w while an increase in Pemetrexed 150399-23-8 blood urea and serum creatinine did not reach statistically significant values. Meanwhile showed diabetic rats with fosinopril were treated, significant inhibition of diabetic kidney damage ending With proteinuria 59.0% lower, the reduction of 27.5% in the mesangial matrix expansion, 31.3% of the tubulointerstitial fewer injuries, althoughIn GC TOF-MS analysis based on metabolic fingerprints of 600 variables with retention time and m / z were detected, of which some 120 metabolites have been identified combined. To the systemic metabolic Ver To see changes between different groups, the partial least squares discriminant analysis model data of all samples was used in our study. As the diagram shows the model established PLSDA score, diabetic animals and controls They were v Llig in the first dimension by the value of isolated 0, indicating that considerable improvements Changes in the metabolic state of rats with local DKD. Fosinopril-treated group exposed.