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10-羧甲基-9-吖啶酮的抗病毒活性

Antiviral activity of 10-carboxymethyl-9-acridanone.

作者信息

Kramer M J, Cleeland R, Grunberg E

出版信息

Antimicrob Agents Chemother. 1976 Feb;9(2):233-8. doi: 10.1128/AAC.9.2.233.

Abstract

Intraperitoneal administration of 10-carboxymethyl-9-acridanone sodium salt (CMA) protected at least 50% of mice tested from otherwise lethal infections with Semliki forest, coxsackie B1, Columbia SK, Western equine encephalitis, herpes simplex, and pseudorabies viruses. The protective effect against influenza A2/Asian/J305 and coxsackie A21 viruses was less but was statistically significant. When administered either subcutaneously or orally, CMA protected at least 50% of mice against Semliki forest and pseudorabies viruses; the effect against coxsackie B1 and herpes simplex viruses was less but was statistically significant. Initiation of treatment could be delayed from 2 to 24 h after infection of mice with coxsackie B1, herpes simplex, Semliki forest, and Western equine encephalitis viruses without loss of an antiviral effect. CMA did not inactivate Semliki forest or coxsackie B1 viruses on contact and was without effect against any of the viruses tested in tissue culture by the tube dilution assay. The humoral antibody response in mice to both influenza virus and sheep erythrocytes was unaffected by CMA. After administration of CMA, an interferon-like substance was induced in mice or mouse cell culture but not in rabbits or rabbit cell culture.

摘要

腹腔注射10 - 羧甲基 - 9 - 吖啶酮钠盐(CMA)可使至少50%接受检测的小鼠免受塞姆利基森林病毒、柯萨奇B1病毒、哥伦比亚SK病毒、西部马脑炎病毒、单纯疱疹病毒和伪狂犬病病毒的致死性感染。对甲型流感病毒A2/亚洲/J305和柯萨奇A21病毒的保护作用较小,但具有统计学意义。皮下或口服CMA时,可使至少50%的小鼠免受塞姆利基森林病毒和伪狂犬病病毒的感染;对柯萨奇B1病毒和单纯疱疹病毒的作用较小,但具有统计学意义。在用柯萨奇B1病毒、单纯疱疹病毒、塞姆利基森林病毒和西部马脑炎病毒感染小鼠后,治疗开始时间可从2小时延迟至24小时,而不丧失抗病毒效果。CMA与塞姆利基森林病毒或柯萨奇B1病毒接触时不会使其灭活,并且在试管稀释试验中对组织培养中测试的任何病毒均无作用。小鼠对流感病毒和绵羊红细胞的体液抗体反应不受CMA影响。给予CMA后,在小鼠或小鼠细胞培养物中可诱导出一种类似干扰素的物质,但在兔或兔细胞培养物中则不会。

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