Caulophine Protects Cardiomyocytes From Oxidative and Ischemic Injury

DOI Web Site PubMed 被引用文献5件 参考文献46件
  • Si Kaiwei
    Department of Pharmacology, Xi’an Jiaotong University School of Medicine, P. R. China Department of Immunology and Pathogen Biology, Xi’an Jiaotong University School of Medicine, P. R. China
  • Liu Juntian
    Department of Pharmacology, Xi’an Jiaotong University School of Medicine, P. R. China
  • He Langchong
    Research and Engineering Center for Natural Medicine, Xi’an Jiaotong University School of Medicine, P. R. China
  • Li Xikuan
    Department of Pharmacology, Xi’an Jiaotong University School of Medicine, P. R. China
  • Gou Wei
    Department of Pharmacology, Xi’an Jiaotong University School of Medicine, P. R. China
  • Liu Chuanhao
    Department of Pharmacology, Xi’an Jiaotong University School of Medicine, P. R. China
  • Li Xiaoqi
    Department of Immunology and Pathogen Biology, Xi’an Jiaotong University School of Medicine, P. R. China

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Caulophine is a new fluorenone alkaloid isolated from the radix of Caulophyllum robustum MAXIM and identified as 3-(2-(dimethylamino) ethyl)-4,5-dihydroxy-1,6-dimethoxy-9H-fluoren-9-one. Due to its new chemical structure, the pharmacological activities of caulophine are not well characterized. The present study evaluated the protective effect and the primary mechanisms of caulophine on cardiomyocyte injury. Viability of cardiomyocytes was assayed with the MTT method, and cell apoptosis was detected by flow cytometry. Myocardial infarction was produced by ligating the coronary artery, and myocardial ischemia was induced by isoproterenol in rats. Myocardial infarction size was estimated with p-nitro-blue tetrazolium staining. Lactate dehydrogenase (LDH), creatine kinase (CK), superoxide dismutase (SOD), malondialdehyde (MDA), and free fatty acid (FFA) were spectrophotometrically determined. Histopathological and ultrastructural changes of ischemic myocardium were observed. The results showed that pretreatment with caulophine increased the viability of H2O2- and adriamycin-injured cardiomyocytes; decreased CK, LDH, and MDA; increased SOD; and inhibited H2O2-induced cellular apoptosis. Caulophine reduced myocardial infarct size and serum CK, LDH, FFA, and MDA; raised serum SOD; and improved histopathological and ultrastructural changes of ischemic myocardium. The results demonstrate that caulophine has the ability to protect cardiomyocytes from oxidative and ischemic injury through an antioxidative mechanism that provides a basis for further study and development of caulophine as a promising agent for treating coronary heart disease.

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