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Overactivation of microglial cells may cause severe brain tissue damage in various neurodegenerative diseases. Therefore, the overactivation of microglia should be repressed by any means. The present study investigated the potential mechanism and signaling pathway for the repressive effect of TGF-beta1, a major anti-inflammatory cytokine, on overactivation and resultant death of microglial cells. A bacterial endotoxin LPS stimulated expression of inducible NO synthase (iNOS) and caused death in

(S)-cis-verbenol, a natural metabolite from (-)-alpha-pinene of host pine tree, has been suggested to have anti-ischemic activity. However, the exact mechanism for the anti-ischemic activity of (S)-cis-verbenol remains unclear yet. In the present study, (S)-cis-verbenol reduced cerebral ischemic injury caused by 1.5-h middle cerebral artery occlusion followed by 24-h reperfusion. Furthermore, (S)-cis-verbenol significantly prevented neuronal cell death caused by oxygen-glucose deprivation (OGD,

S-Allyl-L-cysteine (SAC) has been shown to reduce ischemic injury due to its antioxidant activity. However, the antioxidant property of SAC has been controversial. The present study investigated the neuroprotective mechanism of SAC in cerebral ischemic insults. SAC decreased the size of infarction after transient or global ischemic insults. While it did not alter the N-methyl-D-aspartate excitotoxicity, SAC significantly scavenged the endogenously or exogenously produced ONOO- and reduced ONOO-

In intracerebral hemorrhage, microglia become rapidly activated and remove the deposited blood and cellular debris. To survive in a harmful hemorrhagic or posthemorrhagic condition, activated microglia must be equipped with appropriate self-defensive mechanism(s) to resist the toxicity of hemin, a component released from damaged RBCs. In the current study, we found that activation of microglia by pretreatment with LPS markedly reduced their vulnerability to hemin toxicity in vitro. Similarly, in

In the cerebral ischemic penumbra, progressive metabolic deterioration eventually leads to death of glial cells. The exact mechanism for the death of glial cells is unclear. Here we report that under glucose-deprived conditions immunostimulated glial cells rapidly underwent death via production of large amounts of peroxynitrite. The cell-permeable Mn(III)tetrakis(N-methyl-4'-pyridyl)porphyrin (MnTMPyP) caused a concentration-dependent attenuation of the increased death in glucose-deprived immuno

Astrocytes play an essential role in the maintenance of normal neuronal function. Here we report that pretreatment of interferon-gamma (IFN-gamma) and lipopolysaccharides (LPS) made murine astrocytes highly vulnerable to glucose deprivation-induced death. Neither 12-hr glucose deprivation nor 2-day treatment with IFN-gamma (100 U/ml) and LPS (1 microg/ml) altered the viability of astrocytes. However, significant death of IFN-gamma/LPS-treated astrocytes was observed after 4-hr glucose deprivatio