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己酮可可碱可提高小鼠内毒素休克的存活率,并减少肿瘤坏死因子的形成。

Pentoxifylline increases survival in murine endotoxin shock and decreases formation of tumor necrosis factor.

作者信息

Schade U F

机构信息

Forschungsinstitut Borstel, Institut für Experimentelle Biologie und Medizin, Federal Republic of Germany.

出版信息

Circ Shock. 1990 Jun;31(2):171-81.

PMID:2344657
Abstract

Pentoxifylline (POF) was found to possess high protecting potential in murine endotoxin shock. POF was tested in endotoxic shock in normal, LPS-tolerant, LPS-hyperreactive, and D-galactosamine-sensitized mice. A dose of 50 mg/kg increased survival in normal and tolerant mice from 50% in LPS-controls to 90%, and in LPS-hypersensitized and D-galactosamine-sensitized mice from 20% in LPS-controls to 90%. POF did not interfere with the development of endotoxin tolerance. The protective effects of POF were dose-dependent and were observed, even when POF was given up to 4 h post endotoxin. POF was found to inhibit the appearance of TNF in serum of LPS-treated, D-galactosamine-sensitized mice and in the supernatants of LPS-stimulated, thioglycollate-induced mouse peritoneal macrophages.

摘要

己酮可可碱(POF)被发现对小鼠内毒素休克具有很高的保护潜力。在正常、脂多糖耐受、脂多糖高反应性和D-半乳糖胺致敏的小鼠内毒素休克模型中对POF进行了测试。50mg/kg的剂量可使正常和耐受小鼠的存活率从脂多糖对照组的50%提高到90%,使脂多糖超敏和D-半乳糖胺致敏小鼠的存活率从脂多糖对照组的20%提高到90%。POF不干扰内毒素耐受性的形成。POF的保护作用呈剂量依赖性,即使在内毒素注射后4小时给予POF也可观察到该作用。已发现POF可抑制脂多糖处理的、D-半乳糖胺致敏小鼠血清中以及脂多糖刺激的、巯基乙酸诱导的小鼠腹腔巨噬细胞上清液中TNF的出现。

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