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作 者:Taotao Wei Chang Chen Jingwu Hou Baolu Zhao Wenjuan Xin
机构地区:[1]Chinese Acad Sci, Inst Biophys, Beijing 100101, Peoples R China
出 处:《Chinese Science Bulletin》2000年第5期422-426,共5页
摘 要:The cytotoxic effect of nitric oxide on primarily cultured rat cerebellar granule cells was stuatea, and the mechanisms were discussed. The results showed that nitric oxide donor S-nitroso-N-acetyl-penicillamine (SNAP; 500 (imol/L) could induce apoptosis in immature cultures of cerebellar granule cells. Flow cytometry and HPLC analyses revealed that after treatment with SNAP, the mitochondrial transmembrane potential and the cellular ATP content decreased significantly. Nitric oxide scavenger hemoglobin could effectively prevent the neuronal mitochondria from dysfunction and attenuate apoptosis. The results suggested that nitric oxide activated the apoptotic program by inhibiting the activity of mitochondrial respiratory chain and thus decreasing the cellular ATP content.The cytotoxic effect of nitric oxide on primarily cultured rat cerebellar granule cells was studied, and the mechanisms were discussed. The results showed that nitric oxide donor S-nitroso-N-acetyl-penicillamine (SNAP; 500 μmol/L) could induce apoptosis in immature cultures of cerebellar granule cells. Flow cytometry and HPLC analyses revealed that after treatment with SNAP, the mitochondrial transmembrane potential and the cellular ATP content decreased significantly. Nitric oxide scavenger hemoglobin could effectively prevent the neuronal mitochondria from dysfunction and attenuate apoptosis. The results suggested that nitric oxide activated the apoptotic program by inhibiting the activity of mitochondrial respiratory chain and thus decreasing the cellular ATP content.
关 键 词:CEREBELLAR GRANULE cells APOPTOSIS NITRIC oxide mitochondria.
分 类 号:R741[医药卫生—神经病学与精神病学]
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