Chlorogenic acid regulates the expression of protein phosphatase 2A subunit B in the cerebral cortex of a rat stroke model and glutamate-exposed neurons

• Published in: Laboratory animal research Vol. 40; no. 1; p. 8
• Main Authors: Kang, Ju-Bin, Son, Hyun-Kyoung, Park, Dong-Ju, Jin, Yeung-Bae, Koh, Phil-Ok
• Format: Journal Article
• Language: English
• Published: London BioMed Central 01.03.2024; BMC; 한국실험동물학회
• Subjects: Acids; Apoptosis; Biomedical and Life Sciences; Brain injury; Carotid arteries; Cell cycle; Cell death; Cell signaling; Cerebral blood flow; Cerebral cortex; Cerebral ischemia; Chlorogenic acid; Coffee; Cybernetics; Excitotoxicity; Ischemia; Laboratory animals; Life Sciences; Middle cerebral artery occlusion; Neurons; Neuroprotection; Oxidative stress; Phosphatase; Phosphoprotein phosphatase; PP2A subunit B; Protein phosphatase; Proteins; Stroke; Surgery; Variance analysis; Veins & arteries; 수의학; United States > US; Cerebral ischemia; Chlorogenic acid; Middle cerebral artery occlusion; PP2A subunit B
• ISSN: 2233-7660; 1738-6055; 2233-7660
• DOI: 10.1186/s42826-024-00196-5

Background Ischemic stroke is a serious neurological disorder caused by blockages in cerebral artery. Protein phosphatase 2A (PP2A) is a phosphatase that performs a critical role in cell signaling and growth. PP2A subunit B acts as a neuroprotective agent in the nerve system. Chlorogenic acid, which is mainly found in roasted coffee, has antioxidant, anti-inflammatory, and anti-apoptotic effects. We hypothesized that chlorogenic acid modulates PP2A subunit B expression in ischemic stroke models and glutamate-mediated neurons. Middle artery occlusion (MCAO) surgery was operated and chlorogenic acid (30 mg/kg) or phosphate buffer saline was treated 2 h after MCAO. The cerebral cortex was collected 24 h after surgery and the change of PP2A subunit B expression was analyzed. Glutamate and/or chlorogenic acid were treated in cultured neurons, further study was performed. Results A decrease in PP2A subunit B expression in MCAO animals was identified. Chlorogenic acid alleviated this decrease due to ischemic injury. Moreover, the number of PP2A subunit B-positive cells in the ischemic cerebral cortex was significantly decreased, chlorogenic acid alleviated this decrease. We also found protective effects of chlorogenic acid in neurons exposed to glutamate. Glutamate decreased the expression of PP2A subunit B and chlorogenic acid mitigated this decrease. Our results elucidated that chlorogenic acid performs neuroprotective functions and attenuates the reduction of PP2A subunit B by brain damage and glutamate-mediated excitotoxicity. Conclusions We showed that chlorogenic acid attenuated the decrease of PP2A subunit B in ischemic injury and neurons exposed to glutamate. Since PP2A subunit B contributes to the protection of brain tissue, we can suggest that chlorogenic acid preserves neurons by modulating PP2A subunit B during ischemic damage.