Please use this identifier to cite or link to this item: https://ir.swu.ac.th/jspui/handle/123456789/12297
ชื่อเรื่อง: Proteomics study of the antifibrotic effects of α-mangostin in a rat model of renal fibrosis
ผู้แต่ง: Chaeyklinthes T.
Tiyao V.
Roytrakul S.
Phaonakrop N.
Showpittapornchai U.
Pradidarcheep W.
Keywords: alpha mangostin
antifibrotic agent
bile salt export pump
blood clotting factor 7
bms1 protein
c jun amino terminal kinase interacting protein 3
chemokine receptor CX3CR1
complement component C1r
enolase
FLICE inhibitory protein
glutathione peroxidase 2
homeodomain protein
homeodomain protein Dlx-3
initiation factor
interleukin 1beta converting enzyme
kruppel like factor
kruppel like factor 7
mitogen activated protein kinase 14
osteogenin
protective agent
protein
protein strawberry notch homolog 1
ragulator complex protein lamtor3
t complex protein 1 subunit beta
telomeric repeat binding factor 2
thioacetamide
transcription factor Sox5
transforming growth factor beta
ubiquitin carboxyterminal hydrolase 26
ubiquitin thiolesterase
unclassified drug
animal cell
animal experiment
animal model
animal tissue
antifibrotic activity
Article
bioinformatics
Bowman capsule
collagen fiber
controlled study
drug induced disease
gel liquid chromatography
histopathology
infant
interstitium
kidney fibrosis
kidney tissue
liquid chromatography
liquid chromatography-mass spectrometry
MAPK signaling
nonhuman
nucleotide sequence
polyacrylamide gel electrophoresis
protein analysis
protein expression level
protein fingerprinting
rat
renal protection
tandem mass spectrometry
Wistar rat
วันที่เผยแพร่: 2019
บทคัดย่อ: Renal fibrosis is a consequence of a "faulty" wound-healing mechanism that results in the accumulation of extracellular matrix, which could lead to the impairment of renal functions. α-Mangostin (AM) may prevent the formation of liver fibrosis, but there has yet to be a conclusive investigation of its effect on renal fibrosis. To investigate the renoprotective effect of AM against thioacetamide (TAA)-induced renal fibrosis in rats at the morphological and proteomic levels. We divided 18 male Wistar rats into 3 groups: a control group, a TAA-treated group, and a TAA + AM group. The various agents used to treat the rats were administered intraperitoneally over 8 weeks. Subsequently, the morphology of renal tissue was analyzed by histology using Sirius Red staining and the relative amount of stained collagen fibers quantified using ImageJ analysis. One-dimensional gel liquid chromatography with tandem mass spectrometry (GeLC-MS/MS) was used to track levels of protein expression. Proteomic bioinformatics tools including STITCH were used to correlate the levels of markers known to be involved in fibrosis with Sirius Red-stained collagen scoring. Histology revealed that AM could reduce the relative amount of collagen fibers significantly compared with the TAA group. Proteomic analysis revealed the levels of 4 proteins were modulated by AM, namely CASP8 and FADD-like apoptosis regulator (Cflar), Ragulator complex protein LAMTOR3 (Lamtor3), mitogen-activated protein kinase kinase kinase 14 (Map3k14), and C-Jun-amino-terminal kinase-interacting protein 3 (Mapk8ip3). AM can attenuate renal fibrosis by the suppression of pathways involving Cflar, Lamtor3, Map3k14, and Mapk8ip3. © 2018 Thana Chaeyklinthes et al., published by Sciendo.
URI: https://ir.swu.ac.th/jspui/handle/123456789/12297
https://www.scopus.com/inward/record.uri?eid=2-s2.0-85073233792&doi=10.1515%2fabm-2019-0015&partnerID=40&md5=1ff8184d2ad208722254cf88ddab512e
ISSN: 19057415
Appears in Collections:Scopus 1983-2021

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