Abstract
Inflammation is the cause and/or result of many diseases in peripheral tissues and the central nervous system. Recent findings suggested that inflammation in peripheral tissue induces an inflammatory response in the brain that activates glial cells, which, in turn, induce neuronal cell dysfunction. Therefore, anti-inflammatory compounds are important for the suppression of chronic inflammation and prevention of disease. The present study revealed microglial activation in the hippocampus of the brain two days after the peripheral administration of lipopolysaccharide (LPS). Furthermore, the expression of the synaptic vesicle membrane protein, synaptophysin, in the CA3 stratum lucidum of the hippocampus was down-regulated 7 days after the LPS injection. The administration of tocotrienols, a type of vitamin E, significantly attenuated these changes in the hippocampus. Collectively, the present results demonstrated the spread of peripheral inflammatory responses to the brain, in which glial activation and neuronal dysfunction were induced, while tocotrienols exerted anti-inflammatory effects and protected neurons from damage.
Highlights
Chronic inflammation in peripheral tissue has been implicated in the pathogenesis of many diseases; the suppression of inflammatory responses by components in the daily diet is important
Chronic inflammation has been shown to affect brain function, and exogenous inflammation from peripheral tissue has a negative impact on the brain through the blood-brain barrier (BBB) [4,5]
In vitro and in vivo studies demonstrated that tocotrienols exhibited strong antioxidant and anti-inflammatory activities in peripheral tissue [9,11]
Summary
The activation of immunocompetent cells in the blood, including monocytes, neutrophils, and lymphocytes, by chronic inflammation in peripheral tissue has been shown to stimulate inflammatory responses by vascular endothelial cells, which cross the blood-brain barrier (BBB) and activate glial cells that induce aseptic neuronal cell damage [4,5]. Lipopolysaccharide (LPS), an endotoxin of the outer membrane of Gram-negative bacteria, is often used as an inflammation-induced model both in vitro and vivo. It stimulates Toll-like receptor 4 (TLR4) on the cell surface of immunocompetent cells, which release inflammatory substances, such as cytokines. We examined the effects of tocotrienols in a mouse model of LPS-induced inflammation
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