ArticleLaboratory animal research2022
Chlorogenic acid modulates the ubiquitin-proteasome system in stroke animal model.
Article in Laboratory animal research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Chlorogenic Acid: Characteristics, Neuroprotective Effects, and Potential Mechanisms.Current neuropharmacology · 2026Review
- Polyphenolic metabolites inFrontiers in pharmacology · 2025Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundChlorogenic acid, a phenolic compound, has potent antioxidant and neuroprotective properties. The ubiquitin-proteasome system is an important regulators of neurodevelopment and modulators of neuronal function. This system is associated with neurodevelopment and neurotransmission through degradation and removal of damaged proteins. Activation of the ubiquitin-proteasome system is a critical factor in preventing cell death. We have previously reported a decrease in the activity of the ubiquitin-proteasome system during cerebral ischemia. This study investigated whether chlorogenic acid regulates the ubiquitin-proteasome system in an animal stroke model. In adult rats, middle cerebral artery occlusion (MCAO) surgery was performed to induce focal cerebral ischemia. Chlorogenic acid (30 mg/kg) or normal saline was injected into the abdominal cavity 2 h after MCAO surgery, and cerebral cortex tissues were collected 24 h after MCAO damage.
resultsChlorogenic acid attenuated neurobehavioral disorders and histopathological changes caused by MCAO damage. We identified the decreases in ubiquitin C-terminal hydrolase L1, ubiquitin thioesterase OTUB1, proteasome subunit α type 1, proteasome subunit α type 3, and proteasome subunit β type 4 expression using a proteomics approach in MCAO animals. The decrease in these proteins was alleviated by chlorogenic acid. In addition, the results of reverse transcription-polymerase chain reaction confirmed these changes. The identified proteins were markedly reduced in MCAO damage, while chlorogenic acid prevented these reductions induced by MCAO. The decrease of ubiquitin-proteasome system proteins in ischemic damage was associated with neuronal apoptosis.
conclusionsOur results showed that chlorogenic acid regulates ubiquitin-proteasome system proteins and protects cortical neurons from neuronal damage. These results provide evidence that chlorogenic acid has neuroprotective effects and maintains the ubiquitin-proteasome system in ischemic brain injury.
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