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(P<O.05)。右丙亚胺预处理组升高幅度高于紫杉醇组,与正常组及紫杉醇组比较差异均有统计意义(P<O.05)。16周末联合右丙亚胺组与正常对照组、紫杉醇组比较,SOD降低、MDA升高,差异有统计学意义(P<O.05)。不同剂量右丙亚胺组之间比较差异无统计学意义(P>O.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。
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）. Conelusion The dexrazoxane increase paclitaxel-induced cardiotoxicity through reducing free radical scavenging enzyme activity, resulting in excessive lipid peroxidation products.
出处
《医学研究与教育》
CAS
2013年第2期16-20,共5页
Medical Research and Education
基金
河北省科技厅指令性计划项目(10276105D-89)
关键词
右丙亚胺
恶性肿瘤
紫杉醇
心脏毒性
malignant tumour
paclitaxel
dexrazoxane
cardiotoxicity
