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성연희 한국약용작물학회 2006 韓國藥用作物學會誌 Vol.14 No.2
Paeoniae radix has been widely used for its anti-allergic, anti-inflammatory and analgesic effects, and demonstrated to have anticonvulsant, memory enhancing and anxiolytic activities. The present study was performed to examine the protective effect of methanol extract of Paeoniae radix (PR) from Paeonia Japonica Miyabe et Takeda (Paeoniaceae) on hydrogen peroxide (H2O2)-induced neurotoxicity using cultured rat cerebral cortical neuron. H2O2 produced a concentration-dependent reduction of neuronal viability. PR, over a concentration range of 10 to 100㎍/㎖ showed concentration-dependent decrease of the H2O2 (100 μM)-induced neuronal cell death, as assessed by a 3-[4,5-dimethylthiazol-2-yl]-2,5-di-phenyl-tetrazolium bromide assay and the number of apoptotic nuclei, evidenced by Hoechst 33342 staining. PR (100㎍/㎖) inhibited 100 μM H2O2-induced elevation of the cytosolic Ca2+ concentration ([Ca2+]c), which was measured by a fluorescent dye, fluo-4 AM. PR (50㎍/㎖) inhibited glutamate release into medium induced by 100 μM H2O2, which was measured by HPLC, and generation of reactive oxygen species (ROS). These results suggest that PR 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. Paeoniae radix has been widely used for its anti - allergic, anti - inflammatory and analgesic effects, and demon strated to have anticonvulsant, memory enhancing and anxiolytic activities. The present study was performed to examine the protective effect of methanol extract of Paeoniae radix (PR) from Paeonia Japonica Miyabe et Takeda (Paeoniaceae) on hydro gen peroxide (H 2 O 2 ) - induced neurotoxicity using cultured rat cerebral cortical neuron. H 2 O 2 produced a concentration - depen dent reduction of neuronal viability. PR, over a concentration range of 10 to 100 ㎍ / ㎖ showed concentration - dependent decrease of the H 2 O 2 ( 1 0 0 µ M ) - induced neuronal cell death, as assessed by a 3 - [4,5 - dimethylthiazol - 2 - yl] - 2,5-di - phenyl - tetrazo lium bromide assay and the number of apoptotic nuclei, evidenced by Hoechst 33342 staining. PR (100 ㎍ / ㎖ ) inhibited 100 µM H 2 O 2 - induced elevation of the cytosolic Ca 2+ concentration ([Ca 2+ ] c ), which was measured by a fluorescent dye, fluo - 4 AM. PR (50 ㎍ / ㎖ ) i n h i b i t e d g l u t a m a t e r e l e a s e i n t o m e d i u m i n d u c e d b y 1 0 0 µ M H 2 O 2 , which was measured by HPLC, and generation of reactive oxygen species (ROS). These results suggest that PR may mitigate the H 2 O 2 - induced neurotoxiciy by interfering with the increase of [Ca 2+ ] c , and then inhibiting glutamate release and generation of ROS in cultured neurons.
성연희 충북대학교 동물의학연구소 2022 Journal of Biomedical and Translational Research Vol.23 No.2
Aralia elata, Chaenomeles sinensis fruit, and Glycyrrhizae radix have been widely used as oriental medicinal plants in Korea, China and Japan and found to possess anti-oxidative and anti-inflammatory activities. The current study was conducted to investigate the neuroprotec-tive effect of an ethanol extract of a mixture of A. elata, C. sinensis fruit, and Glycyrrhizae ra-dix (ACG) against ischemia-induced brain injury in rats and excitotoxic and oxidative neuronal death in primarily cultured rat cortical neurons. Transient focal cerebral ischemia was induced by 2 h middle cerebral artery occlusion followed by 24 h reperfusion (MCAO/R) in rats. Oral administration of ACG (10, 25, and 50 mg/kg) 30 min before MCAO, after 1 h of MCAO, and after 1 h of reperfusion reduced MCAO/R-induced brain infarct and edema formation. ACG also inhibited development of behavioral disabilities in MCAO/R-treated rats. Exposure of cultured cortical neurons to 500 μM glutamate for 12 h resulted in neuronal cell death. ACG (1, 10, and 50 μg/mL) inhibited glutamate-induced neuronal death. Furthermore, ACG inhibited 100 μM hydrogen peroxide (H2O2)- and hypoxia-induced neuronal death. These results sug-gest that the neuroprotective effect of ACG against ischemia-induced brain damage might be associated with its anti-excitotoxic and anti-oxidative activity and that ACG may have a thera-peutic role for prevention of neurodegeneration in stroke.
성연희,박주연,조순옥,권순호,김진배,성낙술,배기환,송경식 한국약용작물학회 2005 韓國藥用作物學會誌 Vol.13 No.2
Caulis Bambusae in Taenia is widely used in Korea and China due to its various pharmacological activity. The present study aims to investigate the effect of the methanol extract of Caulis Bambusae in Taenia (CB) from Phyllostachys nigraMunro var. henonis Stapf (Gramineae) on amyloid β protein (25-35) (Aβ (25-35)), a synthetic 25-35 amyloid peptide, -induced neurotoxicity using cultured rat cortical neurons. CB, over a concentration range of 10-50.㎍/㎕.ㅤ, inhibited the Aβ (25-35) (10 μM)-induced neuronal cell death, as assessed by a 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and the number of apoptotic nuclei, evidenced by Hoechst 33342 staining. CB (50.㎍/㎕.ㅤ) inhibited glutamate release into medium induced by 10.μM Aβ (25-35), which was measured by HPLC. Pretreatment of CB (50.ㅤ.㎍/㎕.ㅤ) inhibited 10.μM Aβ (25- .ㅤ 35)-induced elevation of cytosolic calcium concentration ([Ca2+]C), which was measured by a fluorescent dye, fluo-4 AM, and generation of reactive oxygen species. These results suggest that CB prevents Aβ (25-35)-induced neuronal ell damage in vitro. Caulis Bambusae in Taenia is widely used in Korea and China due to its various pharmacological activity. The present study aims to investigate the effect of the methanol extract of Caulis Bambusae in Taenia (CB) from Phyllostachys nigraMunro var. henonis Stapf (Gramineae) on amyloid β protein (25-35) (Aβ (25-35)), a synthetic 25-35 amyloid peptide, -induced neurotoxicity using cultured rat cortical neurons. CB, over a concentration range of 10-50.㎍/㎕.ㅤ, inhibited the Aβ (25-35) (10 μM)-induced neuronal cell death, as assessed by a 3-[4,5-dimethylthiazole-2-yl]-2,5-diphenyl-tetrazolium bromide (MTT) assay and the number of apoptotic nuclei, evidenced by Hoechst 33342 staining. CB (50.㎍/㎕.ㅤ) inhibited glutamate release into medium induced by 10.μM Aβ (25-35), which was measured by HPLC. Pretreatment of CB (50.ㅤ.㎍/㎕.ㅤ) inhibited 10.μM Aβ (25- .ㅤ 35)-induced elevation of cytosolic calcium concentration ([Ca2+]C), which was measured by a fluorescent dye, fluo-4 AM, and generation of reactive oxygen species. These results suggest that CB prevents Aβ (25-35)-induced neuronal ell damage in vitro.