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The Inhibitory Effect Of Resveratrol On Inflammatory Response Induced By Endotoxin In Glial Cell And Its Molecular Mechanism

Posted on:2007-03-24Degree:MasterType:Thesis
Country:ChinaCandidate:X F LuFull Text:PDF
GTID:2144360185490150Subject:Genetics
Abstract/Summary:PDF Full Text Request
Microglia and astrocytes, the two immune-regulatory and inflammatory cells of the central nervous system, are activated in response to injury, infection and a variety of neurodegenerative and neuroinflammatory conditions. Activated microglia and astrocytes produce a host of proinflammatory mediators including tumor necrosis factor (TNF)α, interleukin (IL)-1, IL-6, monocyte chemotactic protein (MCP)-1, and nitric oxide (NO). These molecules are thought to exert toxic effects toward neurons and oligodendrocytes.Resveratrol is a polyphenolic compound found in a large amount of plant species, a number of which are components of the human diet, including mulberries, peanuts, grapes and red wines. Many studies have demonstrated that resveratrol has a variety of pharmacological properties, including anti-oxidation, cancer chemoprevention, cardiovascular protection and anti-inflammation. In monocytes and macrophages, resveratrol inhibits LPS-induced expression of TNF-α, IL-1β, IL-6, MCP-1, inducible nitric oxide synthase (iNOS), and the production of these proinflammatory cytokines and NO. The inhibitory effects of resveratrol are mediated through NF-КB signaling pathway.We examined the effect of resveratrol on LPS-induced expression of TNF-α, IL-1β, IL-6, MCP-1, iNOS and generation of NO in murine microglia and astrocytes and explore the mechanisms involved. Our results showed that resveratrol significantly inhibited the expression of TNF-α, IL-1β, IL-6, MCP-1 and iNOS induced by LPS in murine microglia cell line N9 and primary microlgial. But the effect of resveratrol wasn't parallel in these cells. In murine primary astrocytes, resveratrol inhibited LPS-induced expression of TNF-α,IL-1β,...
Keywords/Search Tags:Resveratrol, Glial cell, Endotoxin, Inflammatory response
PDF Full Text Request
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