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可的松对黄酮乙酸抗肿瘤作用的抑制

Inhibition of antitumor effects of flavone acetic acid by cortisone.

作者信息

Ching L M, Joseph W R, Baguley B C

机构信息

Cancer Research Laboratory, University of Auckland Medical School, New Zealand.

出版信息

Anticancer Res. 1993 Jul-Aug;13(4):1139-41.

PMID:8352536
Abstract

The effect of cortisone (2 mg/mouse) on the effect of the antitumour agent flavone acetic acid (NSC 347512) was measured in four different murine tumours, growing subcutaneously. Response was measured by histological assessment of haemorrhagic necrosis after 24 h, and by assessment of tumour growth delay. In C57B1/6 x DBA/2)F1 hosts, cortisone pre-treatment prevented FAA-induced haemorrhagic necrosis in Lewis lung (sub-line LLTC) tumours but did not inhibit necrosis induction in Colon 38 tumours. Similarly in C3H/HeN mice, cortisone pre-treatment prevented FAA-induced necrosis of Spon-2 and partially prevented necrosis induction in mammary M-16/C tumours. Since corticosteroids are often administered, or generated internally, in the course of clinical treatment, this result has implications for the clinical use of FAA and other compounds, which act on tumour vasculature as part of their antitumour action.

摘要

在四种皮下生长的不同小鼠肿瘤中,测定了可的松(2毫克/小鼠)对抗肿瘤药物黄酮乙酸(NSC 347512)作用的影响。通过24小时后出血性坏死的组织学评估以及肿瘤生长延迟评估来衡量反应。在C57B1/6×DBA/2)F1宿主中,可的松预处理可预防黄酮乙酸诱导的Lewis肺癌(亚系LLTC)肿瘤出血性坏死,但不抑制结肠38肿瘤中的坏死诱导。同样,在C3H/HeN小鼠中,可的松预处理可预防黄酮乙酸诱导的Spon-2坏死,并部分预防乳腺M-16/C肿瘤中的坏死诱导。由于在临床治疗过程中经常给予或体内产生皮质类固醇,该结果对黄酮乙酸和其他作为抗肿瘤作用一部分作用于肿瘤血管的化合物的临床应用具有影响。

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