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作 者:白小强[1] 王新兰[1] 韩小东[1,2] 黄勇攀[3,4]
机构地区:[1]延安大学医学院,陕西延安716000 [2]西安交通大学第二附属医院,陕西西安710049 [3]贵州医科大学药理学教研室,贵州贵阳550004 [4]中南大学湘雅医学院,湖南长沙410078
出 处:《贵州医科大学学报》2016年第12期1430-1434,1443,共6页Journal of Guizhou Medical University
基 金:陕西教育厅科学研究项目(12JK0755);延安市科技惠民项目(2014HM-05)
摘 要:目的:探讨黄芩素(Bai)对柔红霉素(Dox)致小鼠心肌损伤的保护作用,阐明其抗柔红霉素诱导的心肌损伤机制。方法:80只小鼠随机分为5组(n=16):对照组、Dox模型组和Bai高、中、低剂量组(40、20、10 mg/kg),腹腔注射柔红霉素(20 mg/kg)制备小鼠心脏毒性模型,检测心肌ALT、AST、CK、LDH、超氧化物歧化酶(SOD)、丙二醛(MDA)、过氧化氢酶(CAT)及谷胱甘肽还原酶(GSH)水平,电镜观察心肌组织超微结构改变。结果:心电图显示,Dox可导致小鼠心律失常;模型组小鼠心肌酶ALT、AST、CK、LDH水平显著升高,Bai高、中、低剂量组呈剂量依赖下降;模型组小鼠心肌SOD、CAT、GSH活性显著下降,MDA含量增多,Bai高、中、低剂量组呈浓度依赖升高,MDA含量降低;电镜显示Dox组小鼠心肌组织超微结构损伤明显,心肌细胞肿胀,部分肌丝排列紊乱,断裂溶解,线粒体明显肿胀,线粒体嵴断裂消失;Bai高、中、低剂量组小鼠心肌超微结构呈不同程度改善。结论:Bai对Dox致小鼠心肌损伤具有保护作用,其机制可能与其抗氧化活性有关。Objective: To investigate the protective effect of Baicalein(Bai) on the myocardial injury induced by Doxorubicin(Dox) in mice, and to elucidate the mechanism of myocardial injury induced by Dox. Methods: 80 mice were randomly divided into five groups (n = 16 ): control group, Dox model group, high, medium and low Bai dose group (40,20,10 mg/kg). Intraperitoneal injection of Dox (20 mg/kg) was adopted to establish mouse cardiac toxicity model. Myocardial ALT, AST, CK, LDH, superoxide dismutase (SOD), malondialdehyde (MDA), catalase (CAT), glutathione reduc- tase (GSH) level were detected, and electron microscope was used to observe the changes of myocar- dial tissue ultrastructure. Results: ECG showed that DOX could lead to mice arrhythmia. In model group of mice, myocardial enzyme such as ALT, AST, CK, LDH levels were significantly elevated, while in high, medium and low Bai dose group the myocardial enzyme activities showed a dose-depend- ent decline. In the model group, SOD, CAT, GSH activity was significantly decreased, while MDA content increased. In high, medium and low Bai dose group SOD, CAT, GSH activity showed a con- centration-dependent increase, while MDA content decreased. Electron microscope showed that the ultrastructure of myocardial tissue in Dox group was obviously damaged, the myocardial cells were swol- len, some of the muscle fibers arranged in disorder and were broken to dissolution, the mitochondria was obviously swollen, and the the mitochondrial crest disappeared. In high, medium and low Bai dose group, myocardial tissue ultrastmcture improved to different degree. Conclusion: Baicalin can play a protective role on myocardial injury induced by Doxorubicin in mice, and the mechanism may be relat- ed to its antioxidant activity.
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