%0 Journal Article
%T Tetrahydroxystilbene Glucoside Attenuates Neuroinflammation through the Inhibition of Microglia Activation
%A Feng Zhang
%A Yan-Ying Wang
%A Jun Yang
%A Yuan-Fu Lu
%A Jie Liu
%A Jing-Shan Shi
%J Oxidative Medicine and Cellular Longevity
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/680545
%X Neuroinflammation is closely implicated in the pathogenesis of neurological diseases. The hallmark of neuroinflammation is the microglia activation. Upon activation, microglia are capable of producing various proinflammatory factors and the accumulation of these factors contribute to the neuronal damage. Therefore, inhibition of microglia-mediated neuroinflammation might hold potential therapy for neurological disorders. 2,3,5,4¡ä-Tetrahydroxystilbene-2-O-¦Â-D-glucoside (TSG), an active component extracted from Polygonum multiflorum, is reported to be beneficial for human health with a great number of pharmacological properties including antioxidant, free radical-scavenging, anti-inflammation, antilipemia, and cardioprotective effects. Recently, TSG-mediated neuroprotective effects have been well demonstrated. However, the neuroprotective actions of TSG on microglia-induced neuroinflammation are not known. In the present study, microglia BV2 cell lines were applied to investigate the anti-neuroinflammatory effects of TSG. Results showed that TSG reduced LPS-induced microglia-derived release of proinflammatory factors such as TNF¦Á, IL-1¦Â, and NO. Moreover, TSG attenuated LPS-induced NADPH oxidase activation and subsequent reactive oxygen species (ROS) production. Further studies indicated that TSG inhibited LPS-induced NF-¦ÊB signaling pathway activation. Together, TSG exerted neuroprotection against microglia-mediated neuroinflammation, suggesting that TSG might present a promising benefit for neurological disorders treatment. 1. Introduction Central nervous system (CNS) is characterized by an immunologically privileged site due to lack of lymphatic infiltration and the limited inflammatory capacity with the presence of blood-brain barrier [1]. Recently, neuroinflammation has been increasingly implicated in the pathogenesis of neurological disorders, including trauma, stroke, brain infections, ischemia, and neurodegenerative diseases, such as Alzheimer¡¯s disease (AD), Parkinson¡¯s disease (PD), Huntington¡¯s disease (HD), multiple sclerosis, and amyotrophic lateral sclerosis [2]. The hallmark of neuroinflammation is considered to be the activation of glial cells, particular microglia [3]. Microglia are the primary immune cells resident within the CNS and serve as the first line of defense to maintain homeostasis during brain injury or disease occurrence [4]. A wide range of stimuli disrupts brain physiological homeostasis and triggers microglia activation. Once activated, microglia are capable of producing a large number of proinflammatory cytokines such as
%U http://www.hindawi.com/journals/omcl/2013/680545/