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Chlorogenic Acid as a Promising Therapeutic for Multiple Sclerosis: Evidence from an Experimental Autoimmune Encephalomyelitis Model

Authors
Kang, SohiHong, SungmooKim, Joong-SunWang, HongbingMoon, ChangjongShin, Taekyun
Issue Date
Apr-2024
Publisher
BIOLIFE SAS
Keywords
chlorogenic acid; experimental autoimmune encephalomyelitis; multiple sclerosis; neuroinflammation; pro-inflammatory cytokine
Citation
JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS, v.38, no.4, pp 3331 - 3344
Pages
14
Indexed
SCIE
Journal Title
JOURNAL OF BIOLOGICAL REGULATORS AND HOMEOSTATIC AGENTS
Volume
38
Number
4
Start Page
3331
End Page
3344
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/70431
DOI
10.23812/j.biol.regul.homeost.agents.20243804.264
ISSN
0393-974X
1724-6083
Abstract
Background: Chlorogenic acid (CGA), a phenolic compound, is renowned for its capacity as an antioxidant, anti-inflammatory agent, and scavenger of free radicals. Multiple sclerosis (MS) is a chronic autoimmune condition impacting the central nervous system, characterized by demyelination and neuroinflammation. This research delved into the potential therapeutic effects of CGA in experimental autoimmune encephalomyelitis (EAE), an established animal model mirroring MS pathology. Methods: We induced EAE in C57BL/6 mice via immunization with myelin oligodendrocyte glycoprotein 35-55 peptide and conducted daily monitoring to record clinical signs, including paraparesis and body weight changes. We performed histological and molecular analyses on spinal cord tissues to evaluate neurodegeneration and neuroinflammation. Results: Intraperitoneal CGA administration significantly reduced the incidence and severity of EAE paraparesis. Histological analysis showed a significant reduction in inflammatory cell infiltration within the spinal cord parenchyma following EAE induction. CGA treatment substantially downregulated mRNA levels of interleukin-1 beta, interleukin-6, tumor necrosis factor-alpha, and interferon -gamma in the spinal cord tissues. Additionally, CGA treatment resulted in a significant decrease in astrogliosis and microglial/macrophage activation in the spinal cords of EAE mice. Conclusions: Our findings demonstrate that CGA has a therapeutic effect on EAE by modulating pro -inflammatory cytokines. These results CGA as a candidate for MS treatment.
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