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Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis

Emodin, a substance extracted from herbs such as rhubarb, has a protective effect on the central nervous system. However, the potential therapeutic effect of emodin in the context of multiple sclerosis remains unknown. In this study, a rat model of experimental autoimmune encephalomyelitis was estab...

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Autores principales: Cui, Yue-Ran, Bu, Zhong-Qi, Yu, Hai-Yang, Yan, Li-Li, Feng, Juan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer - Medknow 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10075100/
https://www.ncbi.nlm.nih.gov/pubmed/36571359
http://dx.doi.org/10.4103/1673-5374.358612
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author Cui, Yue-Ran
Bu, Zhong-Qi
Yu, Hai-Yang
Yan, Li-Li
Feng, Juan
author_facet Cui, Yue-Ran
Bu, Zhong-Qi
Yu, Hai-Yang
Yan, Li-Li
Feng, Juan
author_sort Cui, Yue-Ran
collection PubMed
description Emodin, a substance extracted from herbs such as rhubarb, has a protective effect on the central nervous system. However, the potential therapeutic effect of emodin in the context of multiple sclerosis remains unknown. In this study, a rat model of experimental autoimmune encephalomyelitis was established by immune induction to simulate multiple sclerosis, and the rats were intraperitoneally injected with emodin (20 mg/kg/d) from the day of immune induction until they were sacrificed. In this model, the nucleotide-binding domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and the microglia exacerbated neuroinflammation, playing an important role in the development of multiple sclerosis. In addition, silent information regulator of transcription 1 (SIRT1)/peroxisome proliferator-activated receptor-alpha coactivator (PGC-1α) was found to inhibit activation of the NLRP3 inflammasome, and SIRT1 activation reduced disease severity in experimental autoimmune encephalomyelitis. Furthermore, treatment with emodin decreased body weight loss and neurobehavioral deficits, alleviated inflammatory cell infiltration and demyelination, reduced the expression of inflammatory cytokines, inhibited microglial aggregation and activation, decreased the levels of NLRP3 signaling pathway molecules, and increased the expression of SIRT1 and PGC-1α. These findings suggest that emodin improves the symptoms of experimental autoimmune encephalomyelitis, possibly through regulating the SIRT1/PGC-1α/NLRP3 signaling pathway and inhibiting microglial inflammation. These findings provide experimental evidence for treatment of multiple sclerosis with emodin, enlarging the scope of clinical application for emodin.
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spelling pubmed-100751002023-04-06 Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis Cui, Yue-Ran Bu, Zhong-Qi Yu, Hai-Yang Yan, Li-Li Feng, Juan Neural Regen Res Research Article Emodin, a substance extracted from herbs such as rhubarb, has a protective effect on the central nervous system. However, the potential therapeutic effect of emodin in the context of multiple sclerosis remains unknown. In this study, a rat model of experimental autoimmune encephalomyelitis was established by immune induction to simulate multiple sclerosis, and the rats were intraperitoneally injected with emodin (20 mg/kg/d) from the day of immune induction until they were sacrificed. In this model, the nucleotide-binding domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome and the microglia exacerbated neuroinflammation, playing an important role in the development of multiple sclerosis. In addition, silent information regulator of transcription 1 (SIRT1)/peroxisome proliferator-activated receptor-alpha coactivator (PGC-1α) was found to inhibit activation of the NLRP3 inflammasome, and SIRT1 activation reduced disease severity in experimental autoimmune encephalomyelitis. Furthermore, treatment with emodin decreased body weight loss and neurobehavioral deficits, alleviated inflammatory cell infiltration and demyelination, reduced the expression of inflammatory cytokines, inhibited microglial aggregation and activation, decreased the levels of NLRP3 signaling pathway molecules, and increased the expression of SIRT1 and PGC-1α. These findings suggest that emodin improves the symptoms of experimental autoimmune encephalomyelitis, possibly through regulating the SIRT1/PGC-1α/NLRP3 signaling pathway and inhibiting microglial inflammation. These findings provide experimental evidence for treatment of multiple sclerosis with emodin, enlarging the scope of clinical application for emodin. Wolters Kluwer - Medknow 2022-10-24 /pmc/articles/PMC10075100/ /pubmed/36571359 http://dx.doi.org/10.4103/1673-5374.358612 Text en Copyright: © Neural Regeneration Research https://creativecommons.org/licenses/by-nc-sa/4.0/This is an open access journal, and articles are distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as appropriate credit is given and the new creations are licensed under the identical terms.
spellingShingle Research Article
Cui, Yue-Ran
Bu, Zhong-Qi
Yu, Hai-Yang
Yan, Li-Li
Feng, Juan
Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis
title Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis
title_full Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis
title_fullStr Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis
title_full_unstemmed Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis
title_short Emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis
title_sort emodin attenuates inflammation and demyelination in experimental autoimmune encephalomyelitis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10075100/
https://www.ncbi.nlm.nih.gov/pubmed/36571359
http://dx.doi.org/10.4103/1673-5374.358612
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