Untargeted metabolomics reveals alterations in metabolites of lipid metabolism and immune pathways in serum of rats after long term oral administration of Amalaki rasayana
Ontology highlight
ABSTRACT:
INSTRUMENT(S): RP_Neg_MS, HILIC_Pos_MS, HILIC_Neg_MS, RP_Pos_MS
PROVIDER: MTBLS867 | MetaboLights | 2019-05-24
REPOSITORIES: MetaboLights
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| 20180824_11170HB.raw.zip | Raw | |||
| 20180824_11468BT.raw.zip | Raw | |||
| 20180824_11468H.raw.zip | Raw | |||
| 20180824_11471CL.raw.zip | Raw | |||
| 20180824_11479B.raw.zip | Raw |
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Project description:NRK cells were exposed to serum-free, 10% FBS (control), 10% serum sampled from rats 24 hours after sham surgery (no kidney injury control), or 10% serum sampled from rats 24 hours after I/R AKI surgery (kidney injury serum). After 48 hours of exposure to serum, the NRK cells were harvested and processed for Agilent microarray We previously conducted a Phase I Clinical Trial in which Mesenchymal Stem/Stromal Cells (MSCs) were administered to patients at risk for developing acute kidney injury (AKI), and which suggested that MSC therapy is safe and effective in preventing both postoperative AKI and progression to CKD. It is well understood that AKI creates an internal environment that adversely affects not only the kidneys but also the function of distant organs and tissues. To study the consequences of the AKI environment on MSCs and renal cells, we developed an in vitro assay of exposing MSCs or cultured tubular cells (NRK Cells) to serum from animals that had AKI, or SHAM surgeries. Compared to SHAM sera, exposure of cells to AKI serum caused increased intra-cellular resazurin reduction, and activation of anti-oxidant genes,
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Project description:This a model from the article:
Mathematical model for the androgenic regulation of the prostate in intact and castrated adult male rats.
Potter LK, Zager MG, Barton HA. Am J Physiol Endocrinol Metab.
2006:91(5):E952-64. 16757547
,
Abstract:
The testicular-hypothalamic-pituitary axis regulates male reproductive system functions. Understanding these regulatory mechanisms is important for assessing the reproductive effects of environmental and pharmaceutical androgenic and antiandrogenic compounds. A mathematical model for the dynamics of androgenic synthesis, transport, metabolism, and regulation of the adult rodent ventral prostate was developed on the basis of a model by Barton and Anderson (1997). The model describes the systemic and local kinetics of testosterone (T), 5alpha-dihydrotestosterone (DHT), and luteinizing hormone (LH), with metabolism of T to DHT by 5alpha-reductase in liver and prostate. Also included are feedback loops for the positive regulation of T synthesis by LH and negative regulation of LH by T and DHT. The model simulates maintenance of the prostate as a function of hormone concentrations and androgen receptor (AR)-mediated signal transduction. The regulatory processes involved in prostate size and function include cell proliferation, apoptosis, fluid production, and 5alpha-reductase activity. Each process is controlled through the occupancy of a representative gene by androgen-AR dimers. The model simulates prostate dynamics for intact, castrated, and intravenous T-injected rats. After calibration, the model accurately captures the castration-induced regression of the prostate compared with experimental data that show that the prostate regresses to approximately 17 and 5% of its intact weight at 14 and 30 days postcastration, respectively. The model also accurately predicts serum T and AR levels following castration compared with data. This model provides a framework for quantifying the kinetics and effects of environmental and pharmaceutical endocrine active compounds on the prostate.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
Potter, Zager, Barton (2006) - version03
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd@auckland.ac.nz
The University of Auckland
Auckland Bioengineering Institute
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
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Project description:The purpose of this study was to investigate whether expression of specific genes in peripheral blood can be used as surrogate marker(s) to detect and distinguish target organ-specific chemical toxicity in rats. Rats were intraperitoneally administered a single, acute dose of a well-established hepatotoxic (acetaminophen) or neurotoxic (methyl parathion) chemical. Administration of acetaminophen (AP) or methyl parathion (MP) in the rats resulted in hepatotoxicity as evidenced from elevated blood transaminase activities or neurotoxicity as evidenced from the inhibition of acetyl cholinesterase activity in the blood, respectively. Microarray analysis of the global gene expression profile of rat blood identified distinct gene expression markers capable of detecting and distinguishing hepatotoxicity and neurotoxicity induced by AP and MP, respectively. Differential expressions of the marker genes specific for hepatotoxicity and neurotoxicity were detectable in the blood much earlier than the appearance of the commonly used clinical markers, serum transaminases and acetyl cholinesterase. In summary, our results demonstrated that blood gene expression markers can detect and distinguish target organ toxicity non-invasively and with higher sensitivity than traditional surrogate markers. Keywords: blood, acetaminophen, methyl parathion, rat, hepatotoxicity, neurotoxicity 38 samples were analyzed in this experiment. 15 rats were intraperitoneally administered acetaminophen (AP), 15 rats were intraperitoneally administered methyl parathion (MP), and 8 rats were intraperitoneally administered vegetable oil. At time intervals of 4, 12, and 24 hours following administration of acetaminophen or methyl parathion, 4 rats per chemical were sacrificed and blood was collected. At the 168-hour time interval, 3 rats per chemical were sacrificed and blood was collected. The control animals were sacrificed at the 24-hour time interval. Therefore, there were four rats in each of the 4-, 12-, and 24-hour time points for each chemical and four control rats for each chemical. Similarly, there were three rats in the 168-hour time interval for each chemical. The groups for each chemical and time interval are labeled as follows: APâcontrolâ4 rats: blood_AP_0_4, blood_AP_0_5, blood_AP_0_33, and blood_AP_0_34 APâ4-hoursâ4 rats: blood_AP_4_35, blood_AP_4_38, blood_AP_4_39, and blood_AP_4_40 APâ12-hoursâ4 rats: blood_AP_12_41, blood_AP_12_42, blood_AP_12_43, and blood_AP_12_45 APâ24-hoursâ4 rats: blood_AP_24_47, blood_AP_24_48, blood_AP_24_49, and blood_AP_24_51 APâ168-hoursâ3rats: blood_AP_168_53, blood_AP_168_54, and blood_AP_168_56 MPâcontrolâ4 rats: blood_MP_0_1, blood_MP_0_2, blood_MP_0_3, and blood_MP_0_ 31 MPâ4-hoursâ4 rats: blood_MP_4_11, blood_MP_4_12, blood_MP_4_13, and blood_MP_4_22 MPâ12-hoursâ4 rats: blood_MP_12_20, blood_MP_12_23, blood_MP_12_24, and blood_MP_12_25 MPâ24-hoursâ4 rats: blood_MP_24_6, blood_MP_24_7, blood_MP_24_9, and blood_MP_24_21 MPâ168-hoursâ3rats: blood_MP_168_26, blood_MP_168_27, and blood_MP_168_29
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