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1.
Braz. J. Pharm. Sci. (Online) ; 55: e17819, 2019. tab, graf
Article in English | LILACS | ID: biblio-1055326

ABSTRACT

Weaning results in intestinal dysfunction, mucosal atrophy, transient anorexia, and intestinal barrier defects. In this study, the effect of prodigiosin (PG) on the intestinal inflammation of weaned rats was investigated by using 1H-NMR spectroscopy and biochemistry indexes to regulate the intestinal metabolism. After administration for 14 days, the body mass of the PG group was increased by 1.29- and 1.26-fold compared with those of the control and alcohol groups, respectively, using a dose of 200 µg PG·kg-1 body weight per day. PG increased organic acid content and decreased moisture, pH values, and free ammonia in feces. In addition, PG alleviated the intestinal inflammation of weaned rats. The analysis of 1H-NMR signal peak attribution and the model validation of metabolic data of feces contents showed that PG significantly affected the metabolism of small molecular compounds in the intestinal tract of weaned rats. This study presents the promising alternative of using PG to alleviate intestinal inflammation effectively in the intestinal tract of weaned rats.


Subject(s)
Animals , Male , Rats , Prodigiosin/adverse effects , Weaning , Biochemistry/classification , Proton Magnetic Resonance Spectroscopy/methods , Inflammation/classification , Anorexia , Dosage/adverse effects , Hydrogen-Ion Concentration , Metabolism/drug effects
2.
Chinese Journal of Preventive Medicine ; (12): 1041-1047, 2017.
Article in Chinese | WPRIM | ID: wpr-809606

ABSTRACT

Objective@#To discuss the potential toxic target organ and the toxic effects and mechanisms of tris (2-chloroethyl) phosphate (TCEP) on SD rats.@*Methods@#40 female SD rats weaning from milk for 21 days, weighted (50±2.3)g were selected as subjects and marked by the weight. They were randomly divided into 4 groups, namely control group, 50 (L), 100 (M) and 250 (H) mg·kg-1·d-1 dose of TCEP group. Each group has 10 rats, and administrated the corresponding dose of drug or vehicle by mouth, quaque die for 60 days. All rats were sacrificed after the last administration. The livers and kidneys were dyed by HE for pathological observation; and the blood samples were collected to analyze the biochemical index. H1-Nuclear Magnetic Resonance (1H-NMR)-based metabolomics methods coupling with histopathogy examination were used to investigate the toxic effects of TCEP.@*Results@#Inflammatory cell infiltration and hepatic necrosis were observed in the liver of TCEP-treated rats. Inflammatory cells invaded and calcification/ossification foci were also found in renal of TCEP-treated rats and tumor hyperplasia were existed in renal tubule in H group. The level of HDL-C in the L, M and H group were separately (1.7±0.09) , (1.5±0.07) and (1.3±0.1) µmol/L, which were all significantly lower than that of control group ( (1.9±0.2) µmol/L) (P<0.05) . The activity of cholinesterase (CHE) in the L, M and H group were separately (918±14.8) , (828±28.6) and (674±36.5) U/L, which were all significantly lower than that of control group ((1056±28.8) µmol/L) (P<0.05). Moreover, The level of creatinine (CRE) in the L, M and H group were separately (29.8±4.6) , (28.9±5.3) and (25.8±6.2) µmol/L, which were all significantly lower than that of control group ((30.2±3.9) µmol/L) (P<0.05). In the H group, the enzyme activities of alanine aminotransferase (ALT), lactate dehydrogenase (LDH), creatine kinase (CK), alkaline phosphatase (ALP) and the contents of total bilirubin (TBIL), glucose (GLU) and uric acid (UA) were all significantly higher than the results in control group. The results of 1H-NMR metabolomics showed that the contents of lactate, glycine, high-density lipoprotein, low-density lipoprotein and phosphatidylcholine in blood of rats would decrease by TCEP exposure, while N-acetylglycoprotein, acetate, alanine, glucose, lipids, lipoproteins and fatty acids would increase.@*Conclusion@#TCEP caused disorders in endogenous energy metabolism, leading to the pathological changes of inflammatory cells infiltration and necrosis in liver and kidney, caused enzyme activity changes of ALT, ALP and the content changes of other liver and kidney injury-related markers.

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