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Modulation of thioredoxin by chlorogenic acid in an ischemic stroke model and glutamate-exposed neurons.
Kang, Ju-Bin; Son, Hyun-Kyoung; Park, Dong-Ju; Jin, Yeung-Bae; Shah, Fawad-Ali; Koh, Phil-Ok.
Afiliação
  • Kang JB; Department of Anatomy and Histology, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, 501 Jinjudaero, Jinju 52828, South Korea.
  • Son HK; Department of Anatomy and Histology, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, 501 Jinjudaero, Jinju 52828, South Korea.
  • Park DJ; Department of Anatomy and Histology, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, 501 Jinjudaero, Jinju 52828, South Korea.
  • Jin YB; Department of Anatomy and Histology, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, 501 Jinjudaero, Jinju 52828, South Korea.
  • Shah FA; Department of Anatomy and Histology, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, 501 Jinjudaero, Jinju 52828, South Korea.
  • Koh PO; Department of Anatomy and Histology, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, 501 Jinjudaero, Jinju 52828, South Korea. Electronic address: pokoh@gnu.ac.kr.
Neurosci Lett ; 825: 137701, 2024 Mar 10.
Article em En | MEDLINE | ID: mdl-38395190
ABSTRACT
Ischemic stroke increases the production of reactive oxygen species (ROS), which can eventually lead to neuronal death. Thioredoxin is a small reductase protein that acts as an eliminator of ROS and protects neurons from brain damage. Chlorogenic acid is known as a phenolic compound that has a neuroprotective effect. We investigated the change of thioredoxin expression by chlorogenic acid in a middle cerebral artery occlusion (MCAO) animal model. Adult rats were injected intraperitoneally with phosphate buffered saline or chlorogenic acid (30 mg/kg) 2 h after MCAO. MCAO damage induced neurological defects and increased ROS and lipid peroxidation levels, however, chlorogenic acid mitigated these changes. MCAO damage reduced thioredoxin expression, which was mitigated by chlorogenic acid treatment. The interaction between thioredoxin and apoptosis signal-regulating kinase 1 (ASK1) was decreased in MCAO animals, chlorogenic acid treatment prevented this decrease. In cultured neurons, chlorogenic acid dose-dependently attenuated glutamate-induced decreases in cell viability and thioredoxin expression. Glutamate toxicity downregulated bcl-2 and upregulated bax, cytochrome c, and caspase-3, however, chlorogenic acid attenuated these changes. The mitigating effect of chlorogenic acid was lower in thioredoxin siRNA-transfected cells than in non-transfected cells. These results provide evidence that chlorogenic acid exerts potent antioxidant and neuroprotective effects through regulation of thioredoxin and modulation of ASK1 and thioredoxin binding in ischemic brain injury. These findings indicate that chlorogenic acid exerts a neuroprotective effect by regulating thioredoxin expression in cerebral ischemia and glutamate exposure conditions.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Isquemia Encefálica / Fármacos Neuroprotetores / Acidente Vascular Cerebral / AVC Isquêmico Limite: Animals Idioma: En Revista: Neurosci Lett Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Coréia do Sul

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Isquemia Encefálica / Fármacos Neuroprotetores / Acidente Vascular Cerebral / AVC Isquêmico Limite: Animals Idioma: En Revista: Neurosci Lett Ano de publicação: 2024 Tipo de documento: Article País de afiliação: Coréia do Sul