Evidence map›Paper›PMID 39141244›Full record

ArticleMolecular biology reports2024

Sofalcone attenuates neurodegeneration in MPTP-induced mouse model of Parkinson's disease by inhibiting oxidative stress and neuroinflammation.

Mulan Chen, Xin He, Yepeng Fan, Lei Xia, Zhifang Dong

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In one paragraph

Article in Molecular biology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Mulan Chen *Growth, Development, and Mental Health of Children and Adolescence Center, Pediatric Research Institute, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Chongqing Key Laboratory of Child Neurodevelopment and Cognitive Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Xin He *Growth, Development, and Mental Health of Children and Adolescence Center, Pediatric Research Institute, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Chongqing Key Laboratory of Child Neurodevelopment and Cognitive Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Yepeng FanGrowth, Development, and Mental Health of Children and Adolescence Center, Pediatric Research Institute, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Chongqing Key Laboratory of Child Neurodevelopment and Cognitive Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Lei XiaGrowth, Development, and Mental Health of Children and Adolescence Center, Pediatric Research Institute, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Chongqing Key Laboratory of Child Neurodevelopment and Cognitive Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China.
Zhifang DongGrowth, Development, and Mental Health of Children and Adolescence Center, Pediatric Research Institute, Ministry of Education Key Laboratory of Child Development and Disorders, National Clinical Research Center for Child Health and Disorders, Chongqing Key Laboratory of Child Neurodevelopment and Cognitive Disorders, Children's Hospital of Chongqing Medical University, Chongqing, 400014, China. zfdong@cqmu.edu.cn.

Funding

CQMU Program for Youth Innovation in Future Medicine W0044National Natural Science Foundation of China 32371030Natural Science Foundation of Chongqing CSTB2022NSCQ-BHX0022Natural Science Foundation of Chongqing CSTB2024NSCQ-LZX0008
6 · The paper itself

Abstract

backgroundParkinson's disease (PD) is a progressive neurodegenerative disorder characterized by oxidative stress and neuroinflammation. Sofalcone (SFC), a chalcone derivative known for its antioxidative and anti-inflammatory properties, is widely used clinically as a gastric mucosa protective agent. However, its therapeutic potential in PD remains to be fully explored. In this study, we investigated the neuroprotective effects of SFC in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD mouse model. METHODS AND

resultsWe found that SFC ameliorated MPTP-induced motor impairments in mice, as assessed by the rotarod and wire tests. Moreover, SFC administration prevented the loss of dopaminergic neurons and striatal degeneration induced by MPTP. Subsequent investigations revealed that SFC reversed MPTP-induced downregulation of NRF2, reduced elevated levels of reactive oxygen species (ROS) and malondialdehyde (MDA), and increased total antioxidant capacity (TAOC). Furthermore, SFC suppressed MPTP-induced activation of microglia and astrocytes, downregulated the pro-inflammatory cytokine TNF-α, and upregulated the anti-inflammatory cytokine IL-4. Additionally, SFC ameliorated the MPTP-induced downregulation of phosphorylation of Akt at Ser473.

conclusionsThis study provides evidence for the neuroprotective effects of SFC, highlighting its antioxidative and anti-inflammatory properties and its role in Akt activation in the PD model. These findings underscore SFC's potential as a promising therapeutic candidate for PD, warranting further clinical investigation.

Indexed as

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineChalconesDisease Models, AnimalNeuroprotective AgentsOxidative StressAnimalsAnti-Inflammatory AgentsAntioxidantsDopaminergic NeuronsMaleMiceMice, Inbred C57BLMicrogliaNeuroinflammatory DiseasesNF-E2-Related Factor 2Parkinson Disease1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridineAnti-Inflammatory AgentsAntioxidantsChalconesNeuroprotective AgentsNF-E2-Related Factor 2Reactive Oxygen SpeciesAktNeuroinflammationNRF2Oxidative stressParkinson’s diseaseSofalcone

Identifiers

PMID39141244

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.