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目的:研究丹红注射液(DH)对抗肿瘤药物多柔吡星(DOX)所致小鼠心肌损伤的保护作用及其机制。方法:通过腋下注射Lewis肺癌细胞建立小鼠实体瘤模型,随机分为4组:模型对照组、DOX组、DH组、DH+DOX组。实验结束,颈臼处死小鼠,无菌分离心肌和肿瘤组织,肿瘤称质量,比色法检测心肌组织中乳酸脱氢酶(LDH)、肌酸激酶(CK)、超氧化物歧化酶(SOD)、过氧化物酶(CAT)和谷胱甘肽过氧化物酶(GPx)的活性及丙二醛(MDA)的含量;流式细胞仪检测心肌细胞内的细胞凋亡、活性氧(ROS)和线粒体膜电位(△Ψm)。结果:与模型对照组相比,DOX和DH+DOX组中肿瘤质量显著下降(P<0.01),且DH对DOX的抗肿瘤作用无显著影响;小鼠心肌组织中LDH和CK活性、细胞凋亡显著增加(P<0.01)。与DOX组相比,DH+DOX组心肌组织中LDH和CK活性、细胞凋亡显著降低(P<0.01),且△Ψm、SOD、CAT与GPx的活性显著增加(P<0.05或P<0.01),MDA含量和ROS生成减少(P<0.01)。结论:腹腔注射DH不影响DOX的抗肺癌作用,但对于DOX介导的心肌损伤具有保护作用,其机制与DH抑制心肌组织氧化应激和稳定△Ψm有关。
Objective: To study the protective effect of Danhong injection (DH) on myocardial injury induced by doxorubicin (DOX) in mice and its mechanism. Methods: The mouse solid tumor model was established by injecting Lewis lung cancer cells into the axilla. The model was randomly divided into 4 groups: model control group, DOX group, DH group and DH + DOX group. At the end of the experiment, the mice were sacrificed in the cervical socket, the myocardium and the tumor were aseptically separated, and the tumors were weighed. The contents of lactate dehydrogenase (LDH), creatine kinase (CK), superoxide dismutase (SOD) (CAT), glutathione peroxidase (GPx) and the content of malondialdehyde (MDA). The apoptosis of cardiomyocytes was detected by flow cytometry. The levels of reactive oxygen species (ROS ) And mitochondrial membrane potential (△ Ψm). Results: Compared with the model control group, the tumor mass in DOX and DH + DOX groups was significantly decreased (P <0.01), and DH had no effect on the antitumor effect of DOX. The activities of LDH and CK in mouse myocardium, Death significantly increased (P <0.01). Compared with DOX group, the activities of LDH and CK in DH + DOX group were significantly decreased (P <0.01) and the activities of △ Ψm, SOD, CAT and GPx were significantly increased (P <0.05 or P <0.01) ), MDA content and ROS production decreased (P <0.01). CONCLUSION: Intraperitoneal injection of DH does not affect the anti-lung cancer effect of DOX, but protects against DOX-induced myocardial injury. Its mechanism is related to the inhibition of oxidative stress and stable △ Ψm of myocardial tissue by DH.