thaliporphine preserves cardiac function of endotoxemic rabbits by both directly and indirectly attenuating nfκb signaling pathwaythaliporphine保存endotoxemic兔子的心脏功能直接或间接地衰减nfκb信号通路.pdfVIP

Thaliporphine Preserves Cardiac Function of Endotoxemic Rabbits by Both Directly and Indirectly Attenuating NFkB Signaling Pathway 1,2,3 4 4. 4. 5 4 A. S. Lee , W. P. Chen , Y. L. Kuo , Y. J. Ho , S. S. Lee , M. J. Su * 1 Division of Cardiology, China Medical University Hospital, No.2, Taichung, Taiwan, 2 L5 Research Center, China Medical University Hospital, No.2, Taichung, Taiwan, 3 China Medical University, No.91, Taichung, Taiwan, 4 Institute of Pharmacology, College of Medicine, National Taiwan University, No.1, Sec.1, Taipei, Taiwan, 5 School of Pharmacy, College of Medicine, National Taiwan University, No.1, Sec.1, Taipei, Taiwan Abstract Cardiac depression in sepsis is associated with the increased morbidity and mortality. Although myofilaments damage, autonomic dysfunction, and apoptosis play roles in sepsis-induced myocardial dysfunction, the underlying mechanism is not clear. All of these possible factors are related to NFkB signaling, which plays the main role in sepsis signaling. Thaliporphine was determined to possess anti-inflammatory and cardioprotective activity by suppressing NFkB signaling in rodents. The purpose of this study is to further prove this protective effect in larger septic animals, and try to find the underlying mechanisms. The systolic and diastolic functions were evaluated in vivo by pressure-volume analysis at different preloads. Both preload-dependent and -independent hemodynamic parameters were performed. Inflammatory factors of whole blood and serum samples were analyzed. Several sepsis-related signaling pathways were also determined at protein level. Changes detected by conductance catheter showed Thaliporphine could recover impaired left ventricular systo