Protective effects of salidroside on hydrogen peroxide-induced apoptosis in SH-SY5Y human neuroblastoma cells

Liquiritigenin inhibits Aβ25–35-induced neurotoxicity and secretion of Aβ1–40 in rat hippocampal neurons

“…Fluorescence intensity was analyzed using a fluorescence spectrophotometer (FOLARstar, BMGLABTech, German) with excitation and emission wavelengths of 488 nm and 526 nm; [Ca 2+ ] i was calculated according to the described method [22] .…”

“…After an overnight incubation, cells were treated with/without liquiritigenin (0.02, 0.2, or 2 μmol/L) for 24 h, followed by addition of 10 μmol/L Aβ [25][26][27][28][29][30][31][32][33][34][35] and further incubation with liquiritigenin for 72 h. For targeted detection of Apbb-1, cells were treated with liquiritigenin (0.02, 0.2, or 2 μmol/L) alone for 24 h, then lysed with 4 °C cell lysis buffer (Beyotime, China) as recommended by the manufacturer. SDS-PAGE and Western blotting were performed according to standard protocols [22] using 40 μg protein per lane. Primary antibodies were as follows: Bcl-2 (Beyotime, China, 1:500 dilution), Bax (Beyotime, China, 1:500 dilution), Ntf-3 (Chemicon, USA, 1:1000 dilution), Apbb-1 (Bioss, China, 1:200 dilution), β-tubulin (Walterson, China, 1:1000 dilution, as internal control) and secondary antibody (goat anti-rabbit or goat anti-mouse IgG-HRP, Zhongshan, China, 1:2000 dilution).…”

H2O2Inhibits Proliferation and Mediates Suppression of Migration via DLC1/RhoA Signaling in Cancer Cells

“…It has been demonstrated that H 2 O 2 induces apoptosis in several cancer cell lines. 150 μΜ H 2 O 2 significantly increases the number of apoptotic neuroblastoma cells SH-SY5Y (Zhang et al, 2007). And the apoptosis is induced by 2 mM H 2 O 2 in glioma cells U251 with reduction of cell viability (Tanaka et al, 2004).…”

Neuroprotective Effect of Taurine against Oxidative Stress-Induced Damages in Neuronal Cells

“…Oxidative stress mediated by reactive oxygen species (ROS) such as hydrogen peroxide (H2O2), superoxide radical (O 2 − ), hydroxyl radical (OH) and peroxynitrate (ONOO − ) can be generated by cell lysis, excitatory amino acids including AMPA (α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid hydrobromide), oxidative burst, DNA damage, oxidative of proteins, peroxidation of lipids and cell death including apoptosis and necrosis (Chandra et al, 2000;Ruffels et al, 2004;Zhang et al, 2007;Zhuang et al, 2007;Lin et al, 2009;Chen et al, 2009). Though, the molecular mechanisms involved in oxidative stress-induced apoptotic neuoronal cell death are complex and remains to be characterized (Canas et al, 2007), therapeutic strategies of preventing ROS production can be useful for the treatment of many neurodegenerative disease.…”

“…Oxidative stress-induced cell damage has been widely involved in the neuronal cell death that is associated with many neurodegenerative disorders including Alzheimer's disease, Parkinson's disease, Huntington's disease, ischemic injury and amyotrophic lateral sclerosis (Ruffels et al, 2004;Zhang et al, 2007;Lin et al, 2009;Chen et al, 2009). Oxidative stress mediated by reactive oxygen species (ROS) such as hydrogen peroxide (H2O2), superoxide radical (O 2 − ), hydroxyl radical (OH) and peroxynitrate (ONOO − ) can be generated by cell lysis, excitatory amino acids including AMPA (α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid hydrobromide), oxidative burst, DNA damage, oxidative of proteins, peroxidation of lipids and cell death including apoptosis and necrosis (Chandra et al, 2000;Ruffels et al, 2004;Zhang et al, 2007;Zhuang et al, 2007;Lin et al, 2009;Chen et al, 2009).…”