CL246,738的体内抗病毒作用是由α干扰素和β干扰素的独立诱导介导的。

The in vivo antiviral effect of CL246,738 is mediated by the independent induction of interferon-alpha and interferon-beta.

作者信息

Sarzotti M, Coppenhaver D H, Singh I P, Poast J, Baron S

机构信息

Department of Microbiology, University of Texas Medical Branch, Galveston 77550.

出版信息

J Interferon Res. 1989 Jun;9(3):265-74. doi: 10.1089/jir.1989.9.265.

DOI:10.1089/jir.1989.9.265

PMID:2545791

Abstract

An interferon (IFN) inducer and immunomodulator, CL246,738 [3,6-bis(2-piperidinoethoxy)acridine trihydrochloride], protected mice from lethal infection with Semliki Forest (SFV) and Banzi (BZV) viruses. A single oral dose of CL246,738 (5-150 mg/kg) administered 24 h before intraperitoneal challenge with SFV or BZV fully protected mice from lethal infection. Dose-dependent levels of circulating IFN peaked at 24 h in the serum and peritoneal fluid of CL246,738-treated mice. The circulating IFN of CL246,738-treated mice consisted of IFN-alpha and was produced by spleen cells. Peritoneal exudate cells (PEC) obtained from CL246,738-treated mice produced IFN-beta. Treatment in vivo with anti-IFN-alpha/beta and anti-IFN-beta reversed the protective effect of CL246,738 against lethal SFV encephalitis.

摘要

一种干扰素（IFN）诱导剂和免疫调节剂CL246,738[3,6 - 双（2 - 哌啶基乙氧基）吖啶三盐酸盐]可保护小鼠免受塞姆利基森林病毒（SFV）和班齐病毒（BZV）的致死性感染。在腹腔注射SFV或BZV前24小时口服单次剂量的CL246,738（5 - 150毫克/千克）可完全保护小鼠免受致死性感染。在接受CL246,738治疗的小鼠的血清和腹腔液中，循环IFN的剂量依赖性水平在24小时达到峰值。接受CL246,738治疗的小鼠的循环IFN由IFN - α组成，由脾细胞产生。从接受CL246,738治疗的小鼠获得的腹腔渗出细胞（PEC）产生IFN - β。用抗IFN - α/β和抗IFN - β进行体内治疗可逆转CL246,738对致死性SFV脑炎的保护作用。