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首页> 外文期刊>Journal of pharmacology & toxicology. >Effect of Protein Depletion on Host and Tumor Response to Paclitaxel in Experimental Animals
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Effect of Protein Depletion on Host and Tumor Response to Paclitaxel in Experimental Animals

机译:蛋白质耗竭对实验动物宿主和肿瘤对紫杉醇应答的影响

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The present study is aimed to examine the possible effects of Protein Malnutrition (PM) on the therapeutic activity and toxicity of paclitaxel in mice implanted with Ehrlich carcinoma cells. Mice that were fed either with standard or low protein diets were treated with a single dose of paclitaxel (10 mg kg~-1, i.p.). Paclitaxel administration increased the tumor growth delay of Ehrlich carcinoma from 2.8 days in protein deficient animals to 4.9 days in normal feeding mice and this represented about 43% increase in tumor growth delay. Furthermore, protein deficiency also interfered with the antitumor activity of paclitaxel. The percent survival of tumor-bearing mice after paclitaxel treatment were 56 and 19% in normal fed and protein deficient animals, respectively. Moreover, Paclitaxel administration increased the serum level of creatine phosphokinase isoenzyme (CPK-MB) in both groups, with maximum effect appeared after 48 h. Seventy two hours later, the levels was reduced to the normal values in normal fed animals while in protein malnourished mice, the activity was found to be high.
机译:本研究旨在检查蛋白质营养不良(PM)对紫杉醇对植入Ehrlich癌细胞的小鼠的治疗活性和毒性的可能影响。用标准剂量或低蛋白饮食喂养的小鼠用单剂量紫杉醇(10 mg kg〜-1,腹腔注射)治疗。紫杉醇的给药将艾氏癌的肿瘤生长延迟从蛋白质缺乏动物的2.8天增加到正常喂养小鼠的4.9天,这表示肿瘤生长延迟增加了约43%。此外,蛋白质缺乏也会干扰紫杉醇的抗肿瘤活性。紫杉醇处理后,荷瘤小鼠在正常饮食和蛋白质缺乏动物中的存活率分别为56%和19%。此外,紫杉醇的给药增加了两组的血清肌酸磷酸激酶同工酶(CPK-MB)的水平,在48小时后效果最大。 72小时后,在正常喂养的动物中该水平降低到正常值,而在蛋白质营养不良的小鼠中发现其活性很高。

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