阿米福汀对阿霉素引起心脏毒性的保护作用

The protection of Amifostine on Adriamycin-induced cardiac toxicity

目的:研究阿米福汀对阿霉素所致大鼠心脏毒性模型的影响。方法:30只SD大鼠随机分成三组,对照组(0.9%NaCl3ml/kg,ip,隔日1次,共6次);阿霉素组(阿霉素3mg/kg,ip,隔日1次,共6次);阿霉素+阿米福汀组(前3次阿霉素给药方法同阿霉素组,后3次在给阿霉素前30min先腹腔注射阿米福汀200mg/kg)。各组均于最后一次给药24h后处死动物。用酶学法测定超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px),离体心脏主动脉逆行灌流,借以PCLAB测定心功能。结果:与阿霉素组相比,阿米福汀+阿霉素组可明显提高大鼠左心室发展压、发展压与心率的乘积和最大收缩/舒张速率;提高心脏和肝脏组织的GSH-Px以及心肌和红细胞提取液SOD活性。结论:阿米福汀对阿霉素所引起的心脏毒性有保护作用,阿米福汀是通过增加清除自由基的酶SOD和GSH-Px的活性和(或)减少自由基的产生达到的。

Objective： To study the effect of Amifostine on Adriamycin （ADM） induced cardiotoxic injury in rats. Methods： 30 SD rats were randomly divided into three groups： control group （0.9% NaCl 3 ml/kg, ip, every other day for 6 times）; ADM treated group （ADM 3 mg/kg, ip, every other day for 6 times）; ADM with Amifostine treated group （first three times as described in ADM treated group, but peritoneal injection with Amifostine 200 mg/kg before 30 min of treatment with ADM in the last three times）. After 24 h at the last injection, killed rats and detected SOD, GSH-Px and left ventricutar function with PCLAB. Results： Amifostine could significantly promoted the degree of LVDP, LVDPxHR and ±dp/dtmax, and advanced the content of GSH-Px in heart and liver as well as, the activity of SOD extracted from cardiac muscle and red cells when ADM treated rats were intervened by Amifostine. Conclusion： Amifostine can increase hemodynamic effect, activities of GSH-Px and SOD. Amifostine can inhibit ADM induced cardiotoxicity. Perhaps the mechanism of protection from ADM is through reducing free radical and/or increasing the activity of SOD and GSH-Px.