Neuroprotective Effects of Baicalein, Wogonin, and Oroxylin A on Amyloid Beta-Induced Toxicity via NF-κB/MAPK Pathway Modulation.

Amyloid beta (Aβ) peptide, one of the most important pathogenic traits of Alzheimer's disease (AD), invokes a cascade of oxidative damage and eventually leads to neuronal death. In the present study, baicalein, wogonin, and oroxylin A, main active flavones in , were evaluated for their neuroprotective effects against Aβ-stimulated damage. All tested compounds decreased Aβ-induced ROS generation and cell cycle arrest.

Sulfhydryl-specific probe for monitoring protein redox sensitivity.

Reactive oxygen species (ROS) regulate various biological processes by modifying reactive cysteine residues in the proteins participating in the relevant signaling pathways. Identification of ROS target proteins requires specific reagents that identify ROS-sensitive cysteine sulfhydryls that differ from the known alkylating agents, iodoacetamide and N-ethylmaleimide, which react nonspecifically with oxidized cysteines including sulfenic and sulfinic acid. We designed and synthesized a novel reagent, methyl-3-nitro-4-(piperidin-1-ylsulfonyl)benzoate (NPSB-1), that selectively and specifically reacts with the sulfhydryl of cysteines in model compounds.

Opuntia ficus-indica attenuates neuronal injury in in vitro and in vivo models of cerebral ischemia.

We examined whether the methanol extract of Opuntia ficus-indica (MEOF) has a neuroprotective action against N-methyl-d-aspartate (NMDA)-, kainate (KA)-, and oxygen-glucose deprivation (OGD)-induced neuronal injury in cultured mouse cortical cells. We also evaluated the protective effect of MEOF in the hippocampal CA1 region against neuronal damage evoked by global ischemia in gerbils. Treatment of neuronal cultures with MEOF (30, 300, and 1000 microg/ml) inhibited NMDA (25 microM)-, KA (30 microM)-, and OGD (50 min)-induced neurotoxicity dose-dependently.

Quercetin attenuates oxygen-glucose deprivation- and excitotoxin-induced neurotoxicity in primary cortical cell cultures.

The possible role of quercetin, a naturally occurring plant flavonoid, in protecting against oxygen-glucose deprivation (OGD)-, excitotoxins-, and free radical-induced neuronal injury in mouse cortical cell cultures was investigated. Pre- and co-treatment with quercetin (100 microM) inhibited 50 min OGD-, 20 microM N-methyl-D-aspartate (NMDA)-, and 50 microM kainate-induced neurotoxicity by 36, 22, and 61%, respectively. Quercetin significantly ameliorated free radical-induced neuronal injury caused by buthionine sulfoximine, sodium nitroprusside, ZnCl(2), and FeCl(2).