摘要
目的探讨三七皂苷防治阿霉素致心肌损伤的效果及作用机制。方法取30只健康SD雄性大鼠,按随机数字表法将大鼠分为空白对照组、低剂量组和高剂量组,各10只。空白对照组采取常规措施处理,低剂量组和高剂量组分别采用50 mg/kg,100 mg/kg三七皂苷进行干预。结果低剂量组与高剂量组乳酸脱氢酶(LDH)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)水平均低于空白对照组(P<0.05),高剂量组LDH,CK,CK-MB水平均低于低剂量组(P<0.05);低剂量组与高剂量组超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化酶(GSH-PX)活性均低于空白对照组(P<0.05),高剂量组SOD,CAT,GSH-PX活性均高于低剂量组(P<0.05)。空白对照组心肌组织结构发生明显变化,组织相对松散,部分组织发生萎缩;低剂量组经过三七皂苷处理后心肌组织形态改变得到显著缓解;高剂量组处理后心肌组织形态变化明显,但略好于空白对照组。结论三七皂苷对阿霉素所致心肌损伤具有良好的防治作用。
Objective To investigate the mechanism of notoginsenoside in preventing and treating myocardial damage in rats induced by adriamycin. Methods Totally 30 healthy male SD rats were randomly divided into the blank control group, low dose group and high dose group,10 cases in each group. The blank control group received routine treatment measures,the low dose group and the high dose group received 50,100 mg/kg notoginsenoside, respectively. Results The levels of LDH, CK and CK-MB in the low dose group and the high dose group were significantly lower than those in the blank control group（ P〈0. 05）, and those indexes in the high dose group were significantly lower than those in the low dose group（ P〈0. 05）. The SOD, CAT and GSH-PX activity in the low dose group and the high dose group were significantly lower than those in the blank control group（ P〈0. 05）, and those indexes in the high dose group were significantly lower than those in the low dose group（ P〈0. 05）. In the blank control group,the myocardial tissue structure changed obviously,the tissue was relatively loose,and some tissues were atrophic. After treatment with notoginsenoside,the morphological changes of myocardial tissue in the low dose group were significantly relieved. After high dose treatment, the morphological changes of myocardial tissue were obvious, but only slightly better than the blank control group. Conclusion Notoginsenoside has good preventive and therapeutic effects on myocardial damage induced by adriamycin.
出处
《中国药业》
CAS
2017年第21期15-17,共3页
China Pharmaceuticals
关键词
三七皂苷
阿霉素
心肌损伤
临床效果
作用机制
大鼠
notoginsenoside
adriamycin
myocardial damage
clinical effect
mechanism
rat
