Zerumbone attenuates lipopolysaccharide-induced activation of BV-2 microglial cells via NF-κB signaling

The brain is considered an immune-privileged organ. However, it has been found that inflammation mediated by microglia, which were once believed to support the brain structure, plays important roles in neuronal cell survival and death. Whether activated microglia has beneficial or detrimental effects on neurons remain controversial. Activated microglia could contribute to maintaining homeostasis in the brain by removing damaged cells. Nonetheless, dysregulation of microglial activation leads to neuronal cell death. Therefore, much attention has been paid to compounds that regulate microglial activation. Zerumbone, a constituent ofZingiber zerumbet, has been reported to exert several biological activities such as anticancer, anti-bacterial, and anti-inflammatory effects. In this study, we aimed to determine the anti-inflammatory effect of zerumbone on lipopolysaccharide-induced activation of BV-2 microglial cells and elucidate the underlying mechanism of action. Zerumbone suppressed nitric oxide and prostaglandin E(2)production induced by lipopolysaccharides through inhibiting the expression of inducible nitric oxide synthase and cyclooxygenase-2. Blocking of mitogen-activated protein kinase and NF-kappa B activation, if not completely, is considered to be due to the anti-inflammatory effect of zerumbone against microglial activation.