<abstract xmlns="http://www.w3.org/1999/xhtml"><sec id="j_abm-2019-0015_s_004_w2aab3b7b2b1b6b1aab1c17b1Aa"><h3>Background</h3><p>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.</p></sec><sec id="j_abm-2019-0015_s_005_w2aab3b7b2b1b6b1aab1c17b2Aa"><h3>Objectives</h3><p>To investigate the renoprotective effect of AM against thioacetamide (TAA)-induced renal fibrosis in rats at the morphological and proteomic levels.</p></sec><sec id="j_abm-2019-0015_s_006_w2aab3b7b2b1b6b1aab1c17b3Aa"><h3>Methods</h3><p>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.</p></sec><sec id="j_abm-2019-0015_s_007_w2aab3b7b2b1b6b1aab1c17b4Aa"><h3>Results</h3><p>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).</p></sec><sec id="j_abm-2019-0015_s_008_w2aab3b7b2b1b6b1aab1c17b5Aa"><h3>Conclusion</h3><p>AM can attenuate renal fibrosis by the suppression of pathways involving Cflar, Lamtor3, Map3k14, and Mapk8ip3.</p></sec></abstract>

BackgroundRenal 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.ObjectivesTo investigate the renoprotective effect of AM against thioacetamide (TAA)-induced renal fibrosis in rats at the morphological and proteomic levels.MethodsWe 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.ResultsHistology 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).ConclusionAM can attenuate renal fibrosis by the suppression of pathways involving Cflar, Lamtor3, Map3k14, and Mapk8ip3.

Proteomics study of the antifibrotic effects of α-mangostin in a rat model of renal fibrosis

Asian Biomedicine

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

BackgroundRenal fibrosis is a consequence of a “faulty” wound-healing mechanism that results in the accumulation of extracellular matrix, which could lead to...

Proteomics study of the antifibrotic effects of α-mangostin in a rat model of renal fibrosis

Article Category: Original article

Publié en ligne: 25 sept. 2019

Pages: 149 - 160

DOI: https://doi.org/10.1515/abm-2019-0015

Mots clés
fibrosis, kidney diseases, alpha-mangostin, proteomics, xanthones

© 2018 Thana Chaeyklinthes et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

Proteomics study of the antifibrotic effects of α-mangostin in a rat model of renal fibrosis

Article Category: Original article

Publié en ligne: 25 sept. 2019

Pages: 149 - 160

DOI: https://doi.org/10.1515/abm-2019-0015

Mots clésfibrosis, kidney diseases, alpha-mangostin, proteomics, xanthones

© 2018 Thana Chaeyklinthes et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 License.

Mots clés
fibrosis, kidney diseases, alpha-mangostin, proteomics, xanthones