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Pkc#cod#x003B4; Activation is Involved in ROS-Mediated Mitochondrial Dysfunction and Apoptosis in Cardiomyocytes Exposed to Advanced Glycation End Products.

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Presentation on theme: "Pkc#cod#x003B4; Activation is Involved in ROS-Mediated Mitochondrial Dysfunction and Apoptosis in Cardiomyocytes Exposed to Advanced Glycation End Products."— Presentation transcript:

1 Pkc#cod#x003B4; Activation is Involved in ROS-Mediated Mitochondrial Dysfunction and Apoptosis in Cardiomyocytes Exposed to Advanced Glycation End Products (Ages) Yang Yao-Chih 1 ;Tsai Cheng-Yen 2, 3 ;Chen Chien-Lin 4 ;Kuo Chia-Hua 5, 6 ;Hou Chien-Wen 5 ;Cheng Shi-Yann 7, 8, 9 ;Aneja Ritu 10 ;Huang Chih-Yang 11 ;Kuo Wei-Wen 1 ; 1 Department of Biological Science and Technology, College of Biopharmaceutical and Food Sciences, China Medical University, Taiwan. 2 Department of Pediatrics, China Medical University Beigang Hospital, Taiwan. 3 School of Chinese Medicine, College of Chinese Medicine, China Medical University, Taiwan. 4 Department of Life Sciences, National Chung Hsing University, Taiwan. 5 Laboratory of Exercise Biochemistry, University of Taipei, Taipei, Taiwan. 6 Graduate Institute of Physical Therapy and Rehabilitation Science, China Medical University, Taiwan. 7 Department of Medical Education and Research and Department of Obstetrics and Gynecology, China Medical University Beigang Hospital, Taiwan. 8 Department of Obstetrics and Gynecology, China Medical University An Nan Hospital, Taiwan. 9 Obstetrics and Gynecology, School of Medicine, China Medical University, Taichung, Taiwan. 10 Department of Biology, Georgia State University, Atlanta, GA 30303, USA. 11 Graduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan ; Graduate Institute of Chinese Medical Science, School of Chinese Medicine, China Medical University, Taichung, Taiwan ; Department of Health and Nutrition Biotechnology, Asia University, Taichung, Taiwan. ; Figure 1. AGE-BSA reduces cell viability, enhanced apoptosis and ROS generation in H9c2 cells in a time- and dose-dependent manner. A Cells were treated with 300 #cod#x003BC;gml of AGE-BSA for different time periods as indicated or non-glycated BSA. Cell viability was determined using MTT assays. B Cells were treated with AGE-BSA at different concentrations as indicated. Levels of apoptosis-related proteins were analyzed by western blotting. These are cropped blots; full-length blots are presented in Suppl. Figure S1. C, D Bar graphs show relative optical densities of the fig. 1B apoptosis and survival protein levels at 24 h. E Intracellular ROS levels of fluorescence intensities of DCF and F the mitochondrial ROS levels of AGE-BSA-exposed cardiac cells at the indicated doses and time periods were examined by flow cytometry. NAC 500 #cod#x003BC;M; rotenone Rote 0.1 #cod#x003BC;M. Bars indicate the mean #cod#x000B1; SEM obtained from experiments performed in triplicate. #cod#x0002A; P #cod#x0003C;0.05, #cod#x0002A;#cod#x0002A; P #cod#x0003C;0.01 and #cod#x0002A;#cod#x0002A;#cod#x0002A; P #cod#x0003C;0.001 compared with the control group; # P #cod#x0003C;0.05 and ## P #cod#x0003C;0.01compared with the 300 #cod#x003BC;gmg group; #cod#x02020; P #cod#x0003C;0.05 when compared with 24 h or 36 h. null,null,0(0),null-null. Doi: /AD


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