Hericium erinaceus Promotes Anti-Inflammatory Effects and Regulation of Metabolites in an Animal Model of Cerebellar Ataxia
Cerebellar ataxia is a neurodegenerative disorder with no definitive treatment. Although previous study demonstrated the neuroprotective effects of ( ), the mechanisms of . treatment on the neuroinflammatory response, neurotransmission, and related metabolites remain largely unknown. We demonstrated...
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Published in: | International journal of molecular sciences Vol. 24; no. 7; p. 6089 |
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Main Authors: | , , , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
Switzerland
MDPI AG
23-03-2023
MDPI |
Subjects: | |
Online Access: | Get full text |
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Summary: | Cerebellar ataxia is a neurodegenerative disorder with no definitive treatment. Although previous study demonstrated the neuroprotective effects of
(
), the mechanisms of
. treatment on the neuroinflammatory response, neurotransmission, and related metabolites remain largely unknown. We demonstrated that 3-AP rats treated with 25 mg/kg
extracts had improved motor coordination and balance in the accelerated rotarod and rod tests. We showed that the
. treatment upregulated the expression of
and
genes to levels comparable to those in the non-3-AP control group. Interestingly, we also observed a significant correlation between
gene expression and rod test performance in the 3-AP saline group, but not in the non-3-AP control or
.+3-AP groups, indicating a relationship between
gene expression and motor balance in the 3-AP rat model. Additionally, we also found that the
. treatment increased mitochondrial COX-IV protein expression and normalized dopamine-serotonin neurotransmission and metabolite levels in the cerebellum of the
.+3-AP group compared to the 3-AP saline group. In conclusion, our findings suggest that the
. treatment improved motor function in the 3-AP rat model, which was potentially mediated through neuroprotective mechanisms involving TGFB2-Smad3 signaling via normalization of neurotransmission and metabolic pathways. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 These authors contributed equally to this work. |
ISSN: | 1422-0067 1661-6596 1422-0067 |
DOI: | 10.3390/ijms24076089 |