Chlorogenic Acid as a Promising Therapeutic for Multiple Sclerosis: Evidence from an Experimental Autoimmune Encephalomyelitis Model
- Authors
- Kang, Sohi; Hong, Sungmoo; Kim, Joong-Sun; Wang, Hongbing; Moon, Changjong; Shin, 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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