-
Proteomics study of the antifibrotic effects of α-mangostin in a rat model of renal fibrosis
- Back
Document Title
Proteomics study of the antifibrotic effects of α-mangostin in a rat model of renal fibrosis
Author
Chaeyklinthes T., Tiyao V., Roytrakul S., Phaonakrop N., Showpittapornchai U., Pradidarcheep W.
Name from Authors Collection
Affiliations
Department of Science, Mahidol University International College, Mahidol University, Nakhon Pathom, 73170, Thailand; Department of Anatomy, Faculty of Medicine, Srinakharinwirot University, Bangkok, 10110, Thailand; National Center for Genetic Engineering and Biotechnology, National Science and Technology Development Agency, Pathum Thani, 12120, Thailand
Type
Article
Source Title
Asian Biomedicine
ISSN
19057415
Year
2019
Volume
12
Issue
4
Page
149-160
Open Access
Hybrid Gold
Publisher
Sciendo
DOI
10.1515/abm-2019-0015
Abstract
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.
Keyword
alpha-mangostin | fibrosis | kidney diseases | Proteomics | xanthones
Industrial Classification
Knowledge Taxonomy Level 1
Knowledge Taxonomy Level 2
Knowledge Taxonomy Level 3
License
CC BY
Rights
Author
Publication Source
Scopus