File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Bushen-Yizhi formula ameliorates mitochondrial dysfunction and oxidative stress via AMPK/Sirt1 signaling pathway in D-gal-induced aging rats.

TitleBushen-Yizhi formula ameliorates mitochondrial dysfunction and oxidative stress via AMPK/Sirt1 signaling pathway in D-gal-induced aging rats.
Authors
KeywordsAMPK/Sirt1 signaling
Bushen-Yizhi formula
D-galactose-induced-aging rats
Inflammation
Metabolomics
Mitochondrial dysfunction
Neurodegeneration
Oxidative stress
Issue Date11-May-2023
PublisherBioMed Central
Citation
Chinese Medicine, 2023, v. 18, n. 1 How to Cite?
Abstract

Background

As a major risk factor for neurodegenerative diseases, aging has become a heavy health care burden worldwide. Age-related decline in mitochondrial function and oxidative stress is strongly associated with neurodegeneration. The previous study demonstrated that Bushen-Yizhi formula (BSYZ), a traditional Chinese medicine formula, is effective in reducing neurodegeneration.

Methods

This study is the first to investigate the effect of BSYZ on D-gal-induced learning memory in rats. Secondly, the potential metabolic mechanism of BSYZ was explored by 1H-NMR metabolomics analysis. Then based on the comparison of differential metabolites implied that BSYZ ameliorated mitochondrial dysfunction through choline metabolic pathway in D-gal-treated rats. Finally, pharmacological validation was conducted to explore the effects of BSYZ on D-gal-induced oxidative stress, neuroinflammation, and neuronal apoptosis.

Results

Our data showed that BSYZ increased aspartate and betaine levels, while decreasing choline levels. Furthermore, BSYZ also increased the proteins level of CHDH and BHMT to regulate choline metabolic pathway. Meanwhile, BSYZ alleviated mitochondrial damage and oxidative stress, including enhanced ATP production and the ratio of NAD+/NADH, reduced the level of MDA, enhanced GSH and SOD activity, upregulated the expressions of p-AMPK, SIRT1 proteins. In addition, BSYZ downregulated the levels of inflammatory cytokines, such as TNF-α, IL-1β and IL-6, as well as suppressed Bcl-2 proteins family dependent apoptosis.

Conclusion

BSYZ treatment effectively rescues neurobehavioral impairment by improving mitochondrial dysfunction, oxidative stress, neuroinflammation and neuroapoptosis via AMPK/SIRT1 pathway in D-gal-induced aging.


Persistent Identifierhttp://hdl.handle.net/10722/340737
ISSN
2023 Impact Factor: 5.3
2023 SCImago Journal Rankings: 0.877
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLiao, Y-
dc.contributor.authorLai, Y-
dc.contributor.authorXu, H-
dc.contributor.authorGao, L-
dc.contributor.authorFu, X-
dc.contributor.authorWang, X-
dc.contributor.authorWang, Q-
dc.contributor.authorShen, J-
dc.contributor.authorFang, J-
dc.contributor.authorFang, S-
dc.date.accessioned2024-03-11T10:46:45Z-
dc.date.available2024-03-11T10:46:45Z-
dc.date.issued2023-05-11-
dc.identifier.citationChinese Medicine, 2023, v. 18, n. 1-
dc.identifier.issn1749-8546-
dc.identifier.urihttp://hdl.handle.net/10722/340737-
dc.description.abstract<h3>Background</h3><p>As a major risk factor for neurodegenerative diseases, aging has become a heavy health care burden worldwide. Age-related decline in mitochondrial function and oxidative stress is strongly associated with neurodegeneration. The previous study demonstrated that Bushen-Yizhi formula (BSYZ), a traditional Chinese medicine formula, is effective in reducing neurodegeneration.</p><h3>Methods</h3><p>This study is the first to investigate the effect of BSYZ on D-gal-induced learning memory in rats. Secondly, the potential metabolic mechanism of BSYZ was explored by <sup>1</sup>H-NMR metabolomics analysis. Then based on the comparison of differential metabolites implied that BSYZ ameliorated mitochondrial dysfunction through choline metabolic pathway in D-gal-treated rats. Finally, pharmacological validation was conducted to explore the effects of BSYZ on D-gal-induced oxidative stress, neuroinflammation, and neuronal apoptosis.</p><h3>Results</h3><p>Our data showed that BSYZ increased aspartate and betaine levels, while decreasing choline levels. Furthermore, BSYZ also increased the proteins level of CHDH and BHMT to regulate choline metabolic pathway. Meanwhile, BSYZ alleviated mitochondrial damage and oxidative stress, including enhanced ATP production and the ratio of NAD<sup>+</sup>/NADH, reduced the level of MDA, enhanced GSH and SOD activity, upregulated the expressions of p-AMPK, SIRT1 proteins. In addition, BSYZ downregulated the levels of inflammatory cytokines, such as TNF-α, IL-1β and IL-6, as well as suppressed Bcl-2 proteins family dependent apoptosis.</p><h3>Conclusion</h3><p>BSYZ treatment effectively rescues neurobehavioral impairment by improving mitochondrial dysfunction, oxidative stress, neuroinflammation and neuroapoptosis via AMPK/SIRT1 pathway in D-gal-induced aging.</p>-
dc.languageeng-
dc.publisherBioMed Central-
dc.relation.ispartofChinese Medicine-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAMPK/Sirt1 signaling-
dc.subjectBushen-Yizhi formula-
dc.subjectD-galactose-induced-aging rats-
dc.subjectInflammation-
dc.subjectMetabolomics-
dc.subjectMitochondrial dysfunction-
dc.subjectNeurodegeneration-
dc.subjectOxidative stress-
dc.titleBushen-Yizhi formula ameliorates mitochondrial dysfunction and oxidative stress via AMPK/Sirt1 signaling pathway in D-gal-induced aging rats.-
dc.typeArticle-
dc.identifier.doi10.1186/s13020-023-00755-3-
dc.identifier.scopuseid_2-s2.0-85159186382-
dc.identifier.volume18-
dc.identifier.issue1-
dc.identifier.eissn1749-8546-
dc.identifier.isiWOS:000985352000001-
dc.identifier.issnl1749-8546-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats