CYTOKINE-STIMULATED HUMAN-IMMUNODEFICIENCY-VIRUS REPLICATION IS INHIBITED BY N-ACETYL-L-CYSTEINE
CYTOKINE-STIMULATED HUMAN-IMMUNODEFICIENCY-VIRUS REPLICATION IS INHIBITED BY N-ACETYL-L-CYSTEINE
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DOI：
10.1073/pnas.87.12.4884
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发表时间：
1990-06-01
影响因子：
11.1
通讯作者：
HERZENBERG, LA
中科院分区：
文献类型：
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作者：
ROEDERER, M;STAAL, FJT;HERZENBERG, LA
我们发现肿瘤坏死因子α对人类免疫缺陷病毒（HIV）具有刺激作用。佛波醇12-肉豆蔻酸酯13-乙酸酯可以通过添加N-乙酰基-L-半胱氨酸(NAC)来抑制。 NAC补充细胞内谷胱甘肽，有效抑制急性感染细胞培养物中肿瘤坏死因子α或佛波酯刺激的HIV复制。 NAC还在体外HIV模型系统中抑制细胞因子增强的HIV长末端重复定向的β-半乳糖苷酶表达。这些结果表明细胞内硫醇水平影响艾滋病毒的产生。此外，因为NAC逆转肿瘤坏死因子α。 NAC 在细胞和动物中都具有毒性，并且是一种众所周知的药物，可以口服给药，对人体没有已知的毒性，这些结果表明 NAC 是一种可能的艾滋病治疗剂。
We show that the stimulation of human immunodeficiency virus (HIV) brought about by tumor necrosis factor .alpha. and phorbol 12-myristate 13-acetate can be inhibited by adding N-acetyl-L-cysteine (NAC). NAC, which replenishes intracellular glutathione, effectively inhibits the tumor necrosis factor .alpha.- or phorbol ester-stimulated replication of HIV in acutely infected cell cultures. NAC also inhibits the cytokine-enhanced HIV long terminal repeat-directed expression of .beta.-galactosidase in in vitro HIV model systems. These results show that intracellular thiol levels influence HIV production. Furthermore, because NAC reverses tumor necrosis factor .alpha. toxicity both in cells and in animals and is a well-known drug that can be administered orally without known toxicity in humans, these results suggest that NAC is a possible therapeutic agent in AIDS.