Acer okamotoanum Inhibit the Hydrogen Peroxide-Induced Oxidative Stress in C6 Glial Cells

Chronic oxidative stress due to the accumulation of reactive oxygen species (ROS) in neuronal cells ultimately leads to neurodegenerative diseases. The use of natural therapies for the prevention of ROS-induced cell damage and for the treatment of neurodegenerative disorders has shown promising results. In this study, we evaluated the neuroprotective effects of the ethyl acetate (EtOAc) fraction of A. Okamotoanum against the hydrogen peroxide (H₂O₂)-induced oxidative stress in C6 glial cells. Results show that cell viability was decreased in cells incubated with H₂O₂, whereas the addition of EtOAc fraction treatments in such cells significantly increased viability. The EtOAc fraction showed the highest inhibitory activity against ROS production and it also decreased the expressions of inflammatory proteins including cyclooxygenase-2, inducible nitric oxide synthase and interleukin-1β. Furthermore, the EtOAc fraction inhibited apoptosis by regulating the protein expressions cleaved caspase

The Neuro-Protective Effect of the Methanolic Extract of Perilla frutescens var. japonica and Rosmarinic Acid against H2O2-Induced Oxidative Stress in C6 Glial Cells

Neurodegenerative diseases are often associated with oxidative damage in neuronal cells. This study was conducted to investigate the neuro-protective effect of methanolic (MeOH) extract of Perilla frutescens var. japonica and its one of the major compounds, rosmarinic acid, under oxidative stress induced by hydrogen peroxide (H2O2) in C6 glial cells. Exposure of C6 glial cells to H2O2 enhanced oxidative damage as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and thiobarbituric acid-reactive substance assays. The MeOH extract and rosmarinic acid prevented oxidative stress by increasing cell viability and inhibiting cellular lipid peroxidation. In addition, the MeOH extract and rosmarinic acid reduced H2O2-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the transcriptional level. Moreover, iNOS and COX-2 protein expression was down-regulated in H2O2-indcued C6 glial cells treated with the MeOH extract and rosmarinic acid. These findings suggest that P. frutescens var. japonica and rosmarinic acid could prevent the progression of neurodegenerative diseases through attenuation of neuronal oxidative stress.

Protective Effect of PKC and Nitric Oxide Affecting Taxol-Induced Cytotoxicity in C6-Gial Cells / 대한해부학회지

Paclitaxel (Taxol) is known as effective drug for inhibition of cell cycle encouraging in human cancer cells. This drug named an antimicrotubule agent which simulate the mitotic arrest towards an apoptosis. The influence of phorbol 12 myristate 13 acetate (PMA) activated protein kinase C (PKC) and nitric oxide (NO) on taxol-induced apoptosis, is poorly understood. To investigate the effects of PMA and NO on the signal transduction in taxol-induced apoptosis in C6-glial cells, the viability and caspase-3 activity of C6-glial cells were analyzed. Pretreatement with PKC activatior (PMA) protected taxol-induced cell death in C6-glial cells, by inhibited caspases-3 activity. On the other hand, the taxol-induced apoptosis was highly enhanced by sodium nitroprusside (SNP) and lipopolysaccharide (LPS), as NO activator. These results suggest that PMA strongly blocks the apoptotic effect of taxol, while nitric oxide has no protective effects in the process of toxol-induced apoptosis in C6-glial cells.

Effects of Seongpungtang on the Nitric oxide Production of C(6) glial cell and Microglia / 대한해부학회지

Nitric oxide (NO) can be either neuroprotective or neurotoxic, depending on the cell type from which it is released and the length and severity of the ischemic insult. In the present study, we investigated the neuroprotective effect of Seongpungtang, a Oriental traditional medicine, on ischemic brain insult by C(6) glial cells and microglia produced NO. O production was induced by lipopolysaccharide (LPS) only or LPS combined with phorbol-12-myristate-13-acetate (PMA) in C(6) glial cell and microglia, and we observed the suppressive effect of Seongpungtang on NO production increased by LPS only or LPS combined with PMA. The cells treated with the water extracts of Seongpungtang at 2 mg/ml does not change the viability. And the water extracts of Seongpungtang significantly suppress the NO production induced by LPS or LPS combined PMA in C(6) glial cells and microglia. To validate the neuroprotective effect of Seongpungtang by suppression of NO production, the microglial cells were treated with NF-kB inhibitor pyrrolidine dithiocarbamate (PDTC), and it is completely decreased the NO production induced by LPS combined with PMA. Moreover, the water extracts of Seongpungtang suppress morphological degeneration by LPS combined with PMA in C(6) glial cell and microglia. These results suggest that the protective effects of the water extracts of Seongpungtang against ischemic brain damages may be mediated by regulation of iNOS during ischemic condition.