Vitis amurensis (VA; Vitaceae) has long been used in oriental herbal medicine. It has been reported that roots and seeds of VA have anti-inflammatory and antioxidant effects. In the present study, the protective effect of ethanol extract from stems and leaves of VA on hydrogen peroxide (H2O2) (100 μm)-induced neuronal cell damage was examined in primary cultured rat cortical neurons. VA (10-100 μg/ml) concentration-dependently inhibited H2O2-induced apoptotic neuronal cell death measured by 3-[4,5-Dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. VA inhibited H2O2-induced elevation of intracellular Ca2+ concentration ([Ca2+]i) and generation of reactive oxygen species (ROS), which were measured by fluorescent dyes. Pretreatment of VA also prevented glutamate release into medium induced by 100 μm H2O2, which was measured by HPLC. These results suggest that VA showed a neuroprotective effect on H2O2-induced neuronal cell death by interfering with H2O2-induced elevation of [Ca2+]i, glutamate release, and ROS generation. This has a significant meaning of finding a new pharmacological activity of stems and leaves of VA in the CNS.

Bacillus subtilis subsp. subtilis는 녹조류인 매생이에서 분리되는 총 생균주 중에서 90%를 차지하고 있다. Bacillus subtilis subsp. subtilis에 대한 항미생물 활성을 50 ppm 수준에서 과산화수소와 NaOCl의 각각의 처리가 전해수 (50 ppm) 보다 유의적 수준에서 높았다. 매생이를 50 ppm의 과산화수소, NaOCl 그리고 전해수로 처리한 후 에서 30일간 일반포장 또는 진공포장에 의한

Dried leaves from Cedrela sinensis A. Juss. (CS), have been observed to possess various pharmacological activity and contain various antioxidant constituents. The protective effect of ethanol extract of CS on hydrogen peroxide (H2O2)-induced neurotoxicity was examined using primary cultured rat cortical neurons in the present study. Exposure of cultured neurons to 100 μM H2O2 caused a significant neuronal death as assessed by a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and Hoechst 33342 staining. The addition of CS, over a concentration range of 10 to 50μg/ml, concentration-dependently prevented the H2O2-induced neuronal apoptotic death. CS (50μg/ml) significantly inhibited H2O2-induced elevation of the cytosolic Ca2+ concentration ([Ca2+]c), which was measured by a fluorescent dye, Fluo-4 AM. CS (30 and 50μg/ml) inhibited glutamate release and generation of reactive oxygen species (ROS) induced by 100μM H2O2. These results suggest that CS may mitigate the H2O2-induced neurotoxiciy by interfering with the increase of [Ca2+]c, and then inhibiting glutamate release and generation of ROS in cultured neurons.