{"title":"细胞因子刺激星形胶质细胞培养的细胞毒性:IL - 6和一氧化氮的作用","authors":"Ozlem Yilmaz, D. Taşkıran, S. Aydar","doi":"10.1002/NRC.20002","DOIUrl":null,"url":null,"abstract":"SUMMARY The cytokines interleukin 1 (IL-l) and tumor necrosis factor alpha (TNF-a), produced by glial cells within the brain, appear to contribute to the neuropathogenesis of several inflammatory neurodegenerative diseases. However, little is known about the mechanism underlying cytokineinduced neurotoxicity. Using astroglial cultures obtained from fetal rat brain, we investigated the effects of lipopolysaccharides (LPS) and cytokines (IL- 1 p and TNF-a). Primary cell cultures treated with LPS, IL-l p plus TNF-a generated substantial amounts of nitric oxide (NO), elevated interleukin 6 (IL-6) levels and caused astroglial injury measured by lactate dehydrogenase (LDH) activity. However, blockade of NO production with nitric oxide synthase (NOS) inhibitors did not affect cell death, suggesting that NO is not responsible for cytokine-induced astroglial cell death under the experimental conditions employed.","PeriodicalId":19198,"journal":{"name":"Neuroscience Research Communications","volume":"38 1","pages":"82-91"},"PeriodicalIF":0.0000,"publicationDate":"2004-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"2","resultStr":"{\"title\":\"Cytotoxicity in cytokine stimulated astrocyte cultures: role of IL‐6 and nitric oxide\",\"authors\":\"Ozlem Yilmaz, D. Taşkıran, S. Aydar\",\"doi\":\"10.1002/NRC.20002\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"SUMMARY The cytokines interleukin 1 (IL-l) and tumor necrosis factor alpha (TNF-a), produced by glial cells within the brain, appear to contribute to the neuropathogenesis of several inflammatory neurodegenerative diseases. However, little is known about the mechanism underlying cytokineinduced neurotoxicity. Using astroglial cultures obtained from fetal rat brain, we investigated the effects of lipopolysaccharides (LPS) and cytokines (IL- 1 p and TNF-a). Primary cell cultures treated with LPS, IL-l p plus TNF-a generated substantial amounts of nitric oxide (NO), elevated interleukin 6 (IL-6) levels and caused astroglial injury measured by lactate dehydrogenase (LDH) activity. However, blockade of NO production with nitric oxide synthase (NOS) inhibitors did not affect cell death, suggesting that NO is not responsible for cytokine-induced astroglial cell death under the experimental conditions employed.\",\"PeriodicalId\":19198,\"journal\":{\"name\":\"Neuroscience Research Communications\",\"volume\":\"38 1\",\"pages\":\"82-91\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2004-03-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"2\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Neuroscience Research Communications\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1002/NRC.20002\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Neuroscience Research Communications","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1002/NRC.20002","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 2
摘要
脑内胶质细胞产生的细胞因子白介素1 (il - 1)和肿瘤坏死因子α (TNF-a)似乎参与了几种炎症性神经退行性疾病的神经发病机制。然而，对细胞因子诱导神经毒性的机制知之甚少。利用从胎鼠脑中获得的星形胶质细胞培养物，我们研究了脂多糖(LPS)和细胞因子(IL- 1p和TNF-a)的作用。用LPS、il - 1 p和TNF-a处理的原代细胞培养产生大量一氧化氮(NO)，升高白细胞介素6 (IL-6)水平，并通过乳酸脱氢酶(LDH)活性测量造成星形胶质细胞损伤。然而，用一氧化氮合酶(NOS)抑制剂阻断NO的产生并不影响细胞死亡，这表明在实验条件下，NO与细胞因子诱导的星形胶质细胞死亡无关。
Cytotoxicity in cytokine stimulated astrocyte cultures: role of IL‐6 and nitric oxide
SUMMARY The cytokines interleukin 1 (IL-l) and tumor necrosis factor alpha (TNF-a), produced by glial cells within the brain, appear to contribute to the neuropathogenesis of several inflammatory neurodegenerative diseases. However, little is known about the mechanism underlying cytokineinduced neurotoxicity. Using astroglial cultures obtained from fetal rat brain, we investigated the effects of lipopolysaccharides (LPS) and cytokines (IL- 1 p and TNF-a). Primary cell cultures treated with LPS, IL-l p plus TNF-a generated substantial amounts of nitric oxide (NO), elevated interleukin 6 (IL-6) levels and caused astroglial injury measured by lactate dehydrogenase (LDH) activity. However, blockade of NO production with nitric oxide synthase (NOS) inhibitors did not affect cell death, suggesting that NO is not responsible for cytokine-induced astroglial cell death under the experimental conditions employed.
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