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目的观察蓝莓花色苷对环磷酰胺致大鼠心脏毒性的保护作用,并探讨其作用机制。方法雄性SD大鼠32只,随机分为对照组、环磷酰胺组和蓝莓花色苷20、80 mg/kg组,连续灌胃14 d后,处死动物,其中第8天环磷酰胺组及蓝莓花色苷组大鼠腹腔注射环磷酰胺100 mg/kg;观察心肌组织病理学改变,采用自动生化分析仪测定大鼠血清酶学指标,采用试剂盒法检测心肌组织丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性,Western blot检测心肌细胞Bcl-2和Bax蛋白表达水平。结果环磷酰胺组大鼠心脏出现心肌细胞肥大、变性坏死、凋亡及炎性细胞浸润等病理变化,而蓝莓花色苷组大鼠心脏病理变化不同程度减轻;与对照组比较,环磷酰胺组大鼠心肌细胞乳酸脱氢酶(LDH)、天门冬氨酸氨基转换酶(AST)、肌酸激酶活性[分别为(314.7±9.2)、(772.5±18.3)、(501.5±13.6)U/L]明显升高,心肌组织SOD活性[(21.2±1.4)U/mg prot]下降,MDA含量[(171.2±12.4)μg/gprot]升高;与环磷酰胺组比较,蓝莓花色苷80 mg/kg组大鼠心肌细胞LDH、AST、肌酸激酶活性[分别为(127.7±7.4)、(411.5±10.3)、(268.6±8.4)U/L]明显下降,心肌组织SOD活性[(26.9±1.3)U/mg prot]升高,MDA含量[(144.9±12.8)μg/g prot]下降。结论蓝莓花色苷对环磷酰胺致大鼠心脏毒性具有一定保护作用,作用机制可能与抗氧化有关。
Objective To observe the protective effect of anthocyanins from blueberry on cardiotoxicity induced by cyclophosphamide in rats and to explore its mechanism. Methods Thirty-two male Sprague-Dawley rats were randomly divided into control group, cyclophosphamide group and blueberry anthocyanin 20,80 mg / kg group. After continuous gavage for 14 days, the animals were sacrificed. Among the 8 days, cyclophosphamide group and blueberry The rats in anthocyanin group were intraperitoneally injected with cyclophosphamide (100 mg / kg). The pathological changes of myocardial tissue were observed. Serum enzymological parameters were measured by automatic biochemical analyzer. The content of malondialdehyde (MDA) The activity of superoxide dismutase (SOD) and the protein expression of Bcl-2 and Bax in cardiomyocytes were detected by Western blot. Results The pathological changes such as hypertrophy, degeneration and necrosis, apoptosis and infiltration of inflammatory cells appeared in the heart of cyclophosphamide-treated rats, and the pathological changes of heart in the blueberry anthocyanin group were alleviated to some extent. Compared with the control group, The activities of lactate dehydrogenase (LDH), aspartate aminotransferase (AST) and creatine kinase in rat myocardial cells were (314.7 ± 9.2), (772.5 ± 18.3) and (501.5 ± 13.6) U / L ] (21.2 ± 1.4) U / mg prot] in myocardial tissue and MDA content [(171.2 ± 12.4) μg / gprot] increased significantly compared with those in cyclophosphamide group (P <0.05). The activities of LDH, AST and creatine kinase in myocardial cells were significantly decreased in [(127.7 ± 7.4), (411.5 ± 10.3) and (268.6 ± 8.4) U / ) U / mg prot], MDA content [(144.9 ± 12.8) μg / g prot] decreased. Conclusion The blueberry anthocyanins have some protective effects on the cardiotoxicity induced by cyclophosphamide in rats. The mechanism may be related to the antioxidation.