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阿霉素刺激犬肾(MDCK)细胞使细胞脂质脱酰基并产生前列腺素。

Adriamycin stimulates canine kidney (MDCK) cells to deacylate cellular lipids and to produce prostaglandins.

作者信息

Ohuchi K, Levine L

出版信息

Prostaglandins Med. 1978 Dec;1(6):433-9. doi: 10.1016/0161-4630(78)90114-3.

Abstract

Dog kidney (MDCK) cells treated with adriamycin (0.5 micrograms/ml) for 1 hr, produced from 2 to 7 times more prostaglandins E2 and F2alpha when measured in culture media 24, 48 and 72 hrs after the treatment. Indomethacin (ID50 less than 2 x 10(-8) M) and cycloheximide (0.5 micrograms/ml) inhibited this adriamycin-stimulated prostaglandin production. The aglycone of adriamycin (0.5 to 5.0 micrograms/ml) had little stimulating effect. Treatment of [3H]arachidonic acid-labeled MDCK cells with adriamycin (0.5 micrograms/ml) for 1 hr also stimulated deacylation of cellular lipids during subsequent incubation. Altered morphology of MDCK cells resulted from such treatment with adriamycin; indomethacin did not inhibit this change, but cycloheximide did.

摘要

用阿霉素(0.5微克/毫升)处理1小时的犬肾(MDCK)细胞,在处理后24、48和72小时于培养基中测量时,产生的前列腺素E2和F2α比未处理细胞多2至7倍。吲哚美辛(半数抑制浓度小于2×10⁻⁸M)和环己酰亚胺(0.5微克/毫升)抑制了这种阿霉素刺激的前列腺素产生。阿霉素的糖苷配基(0.5至5.0微克/毫升)几乎没有刺激作用。用阿霉素(0.5微克/毫升)处理[³H]花生四烯酸标记的MDCK细胞1小时,在随后的孵育过程中也刺激了细胞脂质的脱酰作用。阿霉素的这种处理导致MDCK细胞形态改变;吲哚美辛不抑制这种变化,但环己酰亚胺可以。

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