Caulophine Protects Cardiomyocytes From Oxidative and Ischemic Injury

Abstract

Abstract. 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 H 2 O 2 -and adriamycin-injured cardiomyocytes; decreased CK, LDH, and MDA; increased SOD; and inhibited H 2 O 2 -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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“…The interaction between the effective component 17 and the membrane or membrane receptor was reflected in the vascular CMC model, which suggested that 17 may exert bioactivity in the heart [52]. The deeper study demonstrates that 17 is able to protect cardiomyocytes from oxidative and ischemic injury through an antioxidative mechanism [54] and from caffeine-induced injury via calcium antagonism [51]. …”

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Phosphoenolpyruvate, a glycolytic intermediate, as a cytoprotectant and antioxidant in ex-vivo cold-preserved mouse liver: a potential application for organ preservation

“…Oxidative stress contributes to the development of various injuries and organ damage; ROS, particularly ●OH and O● 2 − , are highly reactive substances that play important roles in some diseases . In clinical transplantation, cold preservation induces oxidative stress and leads to the dysfunction and acute rejection of the graft .…”

“…Oxidative stress contributes to the development of various injuries and organ damage; ROS, particularly •OH and O•2 -, are highly reactive substances that play important roles in some diseases. [17][18][19][20] In clinical transplantation, cold preservation induces oxidative stress and leads to the dysfunction and acute rejection of the graft. [20][21][22][23] During the cold preservation of the grafts, •OH radicals are produced by the Fenton reaction using ferric ion released from the cells, and result in oxidative stress being induced in the graft.…”