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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 5. AGE-BSA-induced cardiomyocyte apoptosis is mediated through ROS-dependent PKC#cod#x003B4; activation. NRVM and H9c2 cells were exposed to AGE-BSA 300 #cod#x003BC;gml for 24 h. Cells were co-treated with bryostatin 1, a PKC#cod#x003B4; activator 100 nM, rottlerin, a PKC#cod#x003B4; inhibitor 3 #cod#x003BC;M, NAC 500 #cod#x003BC;M, Rote 0.1 #cod#x003BC;M, Apo 10 #cod#x003BC;M or siPKC#cod#x003B4; 1 #cod#x003BC;g. A Expression and phosphorylation of PKC#cod#x003B4; and B, C, D apoptosis-related proteins were examined by western blot analyses. These are cropped blots, full-length blots of PKC#cod#x003B4; and pPKC#cod#x003B4; are presented in Suppl. Figure S5. #cod#x003B2;-Actin was used as a loading control. N-acetylcysteine, NAC; Rote, rotenone; APO, apocynin; SC, scramble. null,null,0(0),null-null. Doi: /AD


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