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Protection of Amyloid β Protein (25-35)-induced Neuronal Cell Damage by Methanol Extract of New Stem of Phyllostachys nigra Munro var. henonis Stapf in Cultured Rat Cortical Neuron

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초록

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.

Abstract

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.

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