Acacetin Attenuates Neuroinflammation via Regulation the Response to LPS Stimuli In Vitro and In Vivo

作者：Ha Sang Keun; Moon Eunjung; Lee Pyeongjae; Ryu Jong Hoon; Oh Myung Sook; Kim Sun Yeou^*

来源：Neurochemical Research, 2012, 37(7): 1560-1567.

DOI：10.1007/s11064-012-0751-z

• Acacetin
• Microglia
• Neuroinflammation
• Neuroprotection
• Ischemia

Under normal conditions in the brain, microglia play roles in homeostasis regulation and defense against injury. However, over-activated microglia secrete proinflammatory and cytotoxic factors that can induce progressive brain disorders, including Alzheimer%26apos;s disease, Parkinson%26apos;s disease and ischemia. Therefore, regulation of microglial activation contributes to the suppression of neuronal diseases via neuroinflammatory regulation. In this study, we investigated the effects of acacetin (5,7-dihydroxy-4%26apos;-methoxyflavone), which is derived from Robinia pseudoacacia, on neuroinflammation in lipopolysaccharide (LPS)-stimulated BV-2 cells and in animal models of neuroinflammation and ischemia. Acacetin significantly inhibited the release of nitric oxide (NO) and prostaglandin E-2 and the expression of inducible NO synthase and cyclooxygenase-2 in LPS-stimulated BV-2 cells. The compound also reduced proinflammatory cytokines, tumor necrosis factor-alpha and interleukin-1 beta, and inhibited the activation of nuclear factor-kappa B and p38 mitogen-activated protein kinase. In an LPS-induced neuroinflammation mouse model, acacetin significantly suppressed microglial activation. Moreover, acacetin reduced neuronal cell death in an animal model of ischemia. These results suggest that acacetin may act as a potential therapeutic agent for brain diseases involving neuroinflammation.

• 出版日期2012-7