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Expression of Wnt and NCX1 and its correlation with cardiomyocyte apoptosis in mouse with myocardial hypertrophy

Asian Pacific Journal of Tropical Medicine 2015年第11期8卷 909-914页

作者： Jing He Yi Cai Leiming Luo Rong Wang Department of General Surgery PLA General Hospital

Objective:To study the correlation between expression of Wnt and NCXl and cardiomyocyte apoptosis in mouse with myocardial ***:C57B/16 male mice were given the subcutaneous injection of 1 mg/kg isoprenaline to build the myocardial hypertrophy *** 14 d of model building,mice were executed by cervical vertebra *** ratio of heart weight/body weight(HW/BW) and heart weight/tibia length(HW/TL) was observed and proved using HE staining mat detected the size of eaidiomyocytes.40 male C57B/16 mice were randomly divided into the sham group(normal saline) and model group(isoprenaline),with 20 mice in each *** terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling was applied to detect the cardiomyocyte apoptosis;while Western blot and immunohistochemistry were employed to detect the expression of Wnt and ***,the correlation between these two proteins and cardiomyocyte apoptosis was ***:Compared with the sham group,the ratio of HW/BW and HW/TL was increased in the model group,as well as the bigger and hypertrophied cardiomyocytes,decreased number and increased apoptosis of eaidiomyocytes,and increased positive expression of Wnt3 a,WntSa and NCXl in the cardiac muscle ***,there was positive correlation between the expression of Wnt and NCXl and the cardiomyocyte ***:The expression of Wnt3 a,Wnt5a and NCXl in mouse with myocardial hypertrophy is increased and positively correlated with the cardiomyocyte apoptosis.

关键词： Myocardial hypertrophy Wnt NCX1 Cardiomyocyte apop

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ZYZ451 Protects cardiomyocytes from hypoxia-induced apoptosis by enhancing MnSOD and STAT3 interaction

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中国药理学与毒理学杂志 2015年第S1期29卷 27-28页

作者： Shan-shan LUO Ya-qi SHEN Li-ming MA Xian-feng GU Yi-zhun ZHU Department of Pharmacology School of Pharmacy Fudan University Shanghai 201203 China Department of Medicinal Chemistry School of Pharmacy Fudan University Shanghai 201203 China Department of Pharmacology Loo Yong Lin School of Medicine National University of Singapore Singapore

OBJECTIVE 3,5-Dimethoxy-4-(2-amino-3-prop-2-ynylsulfanyl-propionyl)-benzoic acid 4-guanidino-butyl ester(ZYZ451)showed excellent cardio-protective effects in our previous ***,its therapeutic potential in vivo and the mechanism remained to be ***,we evaluated cardiac protective role of ZYZ451 in post-myocardial infarction(post-MI)rats,and elucidated the underlying *** Neonatal rat ventricular cardiomyoctys(NRVCs)were separated and subjected to pre-deoxidized(1%O2,5%CO2),and serum-free medium for 4h to obtain ischemic *** ROS,MnSOD activity and cell apoptosis were tested to verify the cardiac protective effects of *** and siRNA for Stat3 were used to determine role of Stat3 played in cardio-protective effectes of *** were isolated from NRVCs to determine expression of Stat3 and *** and coimmunoprecipitation were conducted to determine the interaction between MnSOD and *** apply post-MI model in rats,the rats were subjected to ligation of LAD except for control *** vehicle or ZYZ451(1,2or 5mg·kg-1)or mixture of Leonurine and SPRC(15mg·kg-1)was administered 7dbefore and 3more days after the *** at risk(AAR),apoptosis in AAR,LDH and MDA levels,and MnSOD activity and expression were detected to evaluate the cardiac *** mitochondria were isolated to determine MnSOD and Stat3 expression in ischemia,and coimmunoprecipitaion was performed to verify the interaction between MnSOD and Stat3 in *** ZYZ451 prevented hypoxia induced NRVCs apoptosis via increasing MnSOD activity and inhibiting mitochondrial ROS ***,5,15-DPP(STAT3phosphorylation inhibitor)failed to inhibit MnSOD activity,while knockout of STAT3 resulted in significant reduction of MnSOD activity,followed by increased mitochondrial ROS production and cardiomyocytes apoptosis in ***,protective effects of ZYZ451 were blunted in Stat3 deficient

关键词： hypoxia acute myocardial infarction ROS MnSOD apop

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Erythropoietin and diabetes mellitus

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World Journal of Diabetes 2015年第14期6卷 1259-1273页

作者： Kenneth Maiese Cellular and Molecular Signaling

Erythropoietin(EPO) is a 30.4 k Da growth factor and cytokine that governs cell proliferation, immune modulation, metabolic homeostasis, vascular function, and cytoprotection. EPO is under investigation for the treatment of variety of diseases, but appears especially suited for the treatment of disorders of metabolism that include diabetes mellitus(DM). DM and the com-plications of this disease impact a significant portion of the global population leading to disability and death with currently limited therapeutic options. In addition to its utility for the treatment of anemia, EPO can improve cardiac function, reduce fatigue, and improve cognition in patients with DM as well as regulate cellular energy metabolism, obesity, tissue repair and regeneration, apoptosis, and autophagy in experimental models of DM. Yet, EPO can have adverse effects that involve the vasculature system and unchecked cellular proliferation. Critical to the cytoprotective capacity and the potential for a positive clinical outcome with EPO are the control of signal transduction pathways that include protein kinase B, the mechanistic target of rapamycin, Wnt signaling, mammalian forkhead transcription factors of the O class, silent mating type information regulation 2 homolog 1(Saccharomyces cerevisiae), and AMP activated protein kinase. Therapeutic strategies that can specifically target and control EPO and its signaling pathways hold great promise for the development of new and effective clinical treatments for DM and the complications of this disorder.

关键词： Protein kinase B AMP activated protein kinase apop

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