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Allicin regulates Treg/Th17 balance in mice with collagen‐induced arthritis by increasing the expression of MEKK2 protein

To study the role of Allicin in regulating Treg/Th17 ratio in splenic lymphocyte by increasing the expression of MEKK2 protein in MAPK signaling pathway, and to explore the mechanism of immune response in mice with collagen‐induced arthritis (CIA). Mouse CIA model was induced by chicken collagen typ...

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Autores principales: Zhang, Yuling, Gong, Yufang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8116865/
https://www.ncbi.nlm.nih.gov/pubmed/34026055
http://dx.doi.org/10.1002/fsn3.2034
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author Zhang, Yuling
Gong, Yufang
author_facet Zhang, Yuling
Gong, Yufang
author_sort Zhang, Yuling
collection PubMed
description To study the role of Allicin in regulating Treg/Th17 ratio in splenic lymphocyte by increasing the expression of MEKK2 protein in MAPK signaling pathway, and to explore the mechanism of immune response in mice with collagen‐induced arthritis (CIA). Mouse CIA model was induced by chicken collagen type II, and experimental mice were randomly divided into NC group, Model group, and Allicin group. HE staining was used to compare the degree of joint pathological damage in mice of each group, and Masson staining to observe the proliferation of collagen tissue in each group. Flow cytometry detected Treg/Th17 ratio in splenic lymphocytes. Furthermore, RT‐PCR and WB were used to detect the mRNA and protein expression of related transcription factors and inflammatory factors Foxp3, ROR‐γt, and IL‐17A, as well as MEK2 protein expression in splenic lymphocytes. The results showed that Allicin treatment could reduce the severity of arthritis and the proliferation of collagen fibers on the surface of cartilage and bone joints in CIA mice. Compared with NC group, Treg decreased and Th17 increased in spleen lymphocyte of Model group (p < .01); after Allicin treatment, Treg increased while Th17 decreased significantly (p < .01). Meanwhile, MEKK2 protein expression in spleen lymphocyte of Model group decreased compared to that in NC group (p < .01), and MEK2 protein expression increased significantly after Allicin treatment (p < .01). To sum up, the present study suggests that MEKK2 protein plays an important role in the pathogenesis of CIA model. In terms of mechanism, Allicin may play a therapeutic role in rheumatoid arthritis (RA) by increasing the expression of MEKK2 protein and affecting Treg/Th17 ratio.
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spelling pubmed-81168652021-05-20 Allicin regulates Treg/Th17 balance in mice with collagen‐induced arthritis by increasing the expression of MEKK2 protein Zhang, Yuling Gong, Yufang Food Sci Nutr Original Research To study the role of Allicin in regulating Treg/Th17 ratio in splenic lymphocyte by increasing the expression of MEKK2 protein in MAPK signaling pathway, and to explore the mechanism of immune response in mice with collagen‐induced arthritis (CIA). Mouse CIA model was induced by chicken collagen type II, and experimental mice were randomly divided into NC group, Model group, and Allicin group. HE staining was used to compare the degree of joint pathological damage in mice of each group, and Masson staining to observe the proliferation of collagen tissue in each group. Flow cytometry detected Treg/Th17 ratio in splenic lymphocytes. Furthermore, RT‐PCR and WB were used to detect the mRNA and protein expression of related transcription factors and inflammatory factors Foxp3, ROR‐γt, and IL‐17A, as well as MEK2 protein expression in splenic lymphocytes. The results showed that Allicin treatment could reduce the severity of arthritis and the proliferation of collagen fibers on the surface of cartilage and bone joints in CIA mice. Compared with NC group, Treg decreased and Th17 increased in spleen lymphocyte of Model group (p < .01); after Allicin treatment, Treg increased while Th17 decreased significantly (p < .01). Meanwhile, MEKK2 protein expression in spleen lymphocyte of Model group decreased compared to that in NC group (p < .01), and MEK2 protein expression increased significantly after Allicin treatment (p < .01). To sum up, the present study suggests that MEKK2 protein plays an important role in the pathogenesis of CIA model. In terms of mechanism, Allicin may play a therapeutic role in rheumatoid arthritis (RA) by increasing the expression of MEKK2 protein and affecting Treg/Th17 ratio. John Wiley and Sons Inc. 2021-04-07 /pmc/articles/PMC8116865/ /pubmed/34026055 http://dx.doi.org/10.1002/fsn3.2034 Text en © 2021 The Authors. Food Science & Nutrition published by Wiley Periodicals LLC https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Zhang, Yuling
Gong, Yufang
Allicin regulates Treg/Th17 balance in mice with collagen‐induced arthritis by increasing the expression of MEKK2 protein
title Allicin regulates Treg/Th17 balance in mice with collagen‐induced arthritis by increasing the expression of MEKK2 protein
title_full Allicin regulates Treg/Th17 balance in mice with collagen‐induced arthritis by increasing the expression of MEKK2 protein
title_fullStr Allicin regulates Treg/Th17 balance in mice with collagen‐induced arthritis by increasing the expression of MEKK2 protein
title_full_unstemmed Allicin regulates Treg/Th17 balance in mice with collagen‐induced arthritis by increasing the expression of MEKK2 protein
title_short Allicin regulates Treg/Th17 balance in mice with collagen‐induced arthritis by increasing the expression of MEKK2 protein
title_sort allicin regulates treg/th17 balance in mice with collagen‐induced arthritis by increasing the expression of mekk2 protein
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8116865/
https://www.ncbi.nlm.nih.gov/pubmed/34026055
http://dx.doi.org/10.1002/fsn3.2034
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