Journal
PHARMACEUTICAL BIOLOGY
Volume 46, Issue 9, Pages 579-586Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/13880200802179659
Keywords
cytokines; ERKs; lipopolysaccharide; lycopene; microglia; NO
Funding
- National Science Council of Taiwan [94-2321-B-038-001]
- Shin Kong Wu Ho-Su Memorial Hospital [SKH-TMU-92-27]
- Min-Sheng Healthcare [93MSH-TMU-10]
- Ministry of Education, Taiwan
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Microglia are activated in response to brain injury and release neurotoxic factors including nitric oxide (NO) and proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). Lycopene, a potent antioxidant, is known to inhibit brain injury. In this study, we found that lycopene (5-20 mu M) significantly inhibited lipopolysaccharide (LPS)-induced NO release in primary cultured microglia. Lycopene (5-20 mu M) also concentration-dependently diminished the LPS-induced production of proinflammatory cytokines such as TNF-alpha and IL-1 beta in microglia. Further study of the molecular mechanisms revealed that lycopene markedly inhibited extracellular signal-regulated kinase (ERK1/2) but not c-Jun N-terminal kinase (JNK1/2) or p38 mitogen-activated protein kinase (MAPK) phosphorylation stimulated by LPS in microglia. These results suggest that microglial inactivation by lycopene is at least partially due to activation of ERK1/2 phosphorylation Therefore, inhibition of NO and proinflammatory cytokine production in activated microglia by lycopene may represent a powerful and potential therapeutic strategy for various neurodegenerative diseases including ischemia-reperfusion cerebral infarction.
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