医学研究与教育 ›› 2013, Vol. 30 ›› Issue (2): 16-20.

• 基础研究 • 上一篇    下一篇

右丙亚胺对紫杉醇所致心脏损伤影响

王佳佳1,臧爱民2,霍然2   

  1. 1.河北大学研究生学院,河北 保定 071000
    2.河北大学附属医院肿瘤内科,河北 保定 071000
  • 收稿日期:2016-10-09 修回日期:2016-10-09 出版日期:2013-04-25 发布日期:2013-04-25

Effects of dexrazoxane for paclitaxel-induced cardiotoxicity

  • Received:2016-10-09 Revised:2016-10-09 Online:2013-04-25 Published:2013-04-25

摘要: 目的探讨右丙亚胺对紫杉醇所致心脏毒性是否具有防治效果及可能机制.方法64只Wistar大鼠随机分为正常对照组、紫杉醇组、紫杉醇+低剂量右丙亚胺组、紫杉醇+高剂量右丙亚胺组.分别于用药第8周末及16周末每组处死大鼠各8只,测定血清肌钙蛋白I( cTnI)、脑钠肽( BNP)、超氧化物歧化酶(SOD)、丙二醛(MDA)水平,比较其中的差异.结果8周末各组之间血清cTnI、BNP、SOD、MDA比较,差异无统计意义(P>O.05).16周末紫杉醇组血清cTnI和BNP含量较正常组升高,差异有统计意义(PO.05).结论右丙亚胺联合紫杉醇可能会降低体内清除自由基的酶的活性,产生过多的脂质过氧化产物,加重紫杉醇所致的心脏毒性.

关键词: 右丙亚胺, 恶性肿瘤, 紫杉醇, 心脏毒性

Abstract: Objective To study the effects of dexrazoxane in preventing paclitaxel-induced cardiotoxicity in rat models and its mechanism. Methods 64 Wistar rats were randomly divided into four groups: Control group, paclitaxel group, paclitaxel + small dose of dexrazoxane group, paclitaxel + large dose of dexrazoxane group. The cardiotoxicity was assessed by measuring serum cardiac troponinl (cTnI), brain natriuretic peptide (BNP), superoxide dismutase (SOD) and malondialdehyde (MDA) at the end of the 8th and 16th weeks. Results At the end of the 8th weeks the differences for cTnI, BNP, SOD, MDA, pathological performance between groups was not statistically significant (P>0.05). At the end of the 16th weeks paclitaxel increased serum cTnI and BNP (P<0.05). The dexrazoxane acceleration the increasing cTnI and BNP (P<0.05). Dexrazoxane + paclitaxel reduce SOD, increased MDA, the difference was statistically significant (P<0.05). The comparison between the different doses of dexrazoxane group was not statistically significant (P>0.05). conclusion The dexrazoxane increase paclitaxel-induced cardiotoxicity through reducing free radical scavenging enzyme activity, resulting in excessive lipid peroxidation products.

Key words: malignant tumour, paclitaxel, dexrazoxane, cardiotoxicity

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