Personalized medicine in Type 2 Diabetes

Liao, Wen Ling; Tsai, Fuu Jen

doi:10.7603/s40681-014-0008-z

Cited by 31 publications

(20 citation statements)

References 53 publications

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“…In addition to controlling the cardiac‐apoptosis, promoting the cell survival mechanism such as those involving insulin‐like growth factor‐I (IGF‐I) signaling pathways, mitogen‐activated protein kinases (MAPK)/extracellular signal‐regulated kinases (ERK) and phosphatidylinositol 3′‐kinase (PI3K)‐protein kinase B (Akt) is an important strategy in treating DM related cardiac‐dysfunction. Various alternative medicines with such potential are been extensively studied and reported …”

Section: Introductionmentioning

confidence: 99%

Cellular apoptosis and cardiac dysfunction in STZ‐induced diabetic rats attenuated by anthocyanins via activation of IGFI‐R/PI3K/Akt survival signaling

Huang

Wang

Fan

et al. 2017

Environmental Toxicology

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Anthocyanins are known cyto-protective agents against various stress conditions. In this study cardio-protective effect of anthocyanins from black rice against diabetic mellitus (DM) was evaluated using a streptozotocin (STZ)-induced DM rat model. Five-week-old male Wistar rats were administered with STZ (55 mg kg , IP) to induce DM; rats in the treatment group received 250 mg oral anthocyanin/kg/day during the 4-week treatment period. DM and the control rats received normal saline through oral gavage. The results reveal that STZ-induced DM elevates myocardial apoptosis and associated proapoptotic proteins but down-regulates the proteins of IGF1R mediated survival signaling mechanism. Furthermore, the functional parameters such as the ejection-fraction and fraction-shortening in the DM rat hearts declined considerably. However, the rats treated with anthocyanins significantly reduced apoptosis and the associated proapoptotic proteins and further increased the survival signals to restore the cardiac functions in DM rats. Anthocyanin supplementation enhances cardiomyocyte survival and restores cardiac function.

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Section: Introductionmentioning

confidence: 99%

Cellular apoptosis and cardiac dysfunction in STZ‐induced diabetic rats attenuated by anthocyanins via activation of IGFI‐R/PI3K/Akt survival signaling

Huang

Wang

Fan

et al. 2017

Environmental Toxicology

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“…Various alternative medicines are been evaluated for their potential to establish cardiac protection . Our previous studies and several other reports show that activation of pJNK and p38 MAPKs play an important role in cardiac hypertrophic effects and associated apoptosis .…”

Section: Discussionmentioning

confidence: 99%

Oolong tea prevents cardiomyocyte loss against hypoxia by attenuating p‐JNK mediated hypertrophy and enhancing P‐IGF1R, p‐akt, and p‐Bad^ser136 activity and by fortifying NRF2 antioxidation system

Shibu

Kuo

Chen

et al. 2017

Environmental Toxicology

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Tea, the most widely consumed natural beverage has been associated with reduced mortality risk from cardiovascular disease. Oolong tea is a partially fermented tea containing high levels of catechins, their degree of oxidation varies between 20%-80% causing differences in their active metabolites. In this study we examined the effect of oolong tea extract (OTE) obtained by oxidation at low-temperature for short-time against hypoxic injury and found that oolong tea provides cyto-protective effects by suppressing the JNK mediated hypertrophic effects and by enhancing the innate antioxidant mechanisms in neonatal cardiomyocytes and in H9c2 cells. OTE effectively attenuates 24 h hypoxia-triggered cardiomyocyte loss by suppressing caspase-3-cleavage and apoptosis in a dose-dependent manner. OTE also enhances the IGFIR/p-Akt associated survival-mechanism involving the elevation of p-Bad in a dose-dependent manner to aid cellular adaptations against hypoxic challenge. The results show the effects and mechanism of Oolong tea to provide cardio-protective benefits during hypoxic conditions.

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“…The incidence of DM in the world has recently speedily evolved. High levels of blood glucose resulting from diabetes increase ROS production in many tissues, leading to the pathogenesis of multitissue damage, such as retinopathy, atherosclerosis, insulin resistance, and cardiomyopathy [Huang and Lee, 2012;Liao and Tsai, 2014]. Among these conditions, cardiomyopathy is the main factor in disability and mortality in diabetic patients [Naqshbandi et al, 2008;Falcao-Pires and Leite-Moreira, 2012].…”

Section: Discussionmentioning

confidence: 99%

Nrf2 Activation as a Protective Feedback to Limit Cell Death in High Glucose‐Exposed Cardiomyocytes

Tsai

Cheng

et al. 2017

J of Cellular Biochemistry

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Hyperglycemia leads to excess reactive oxygen species (ROS) generation, which causes many diabetic complications, such as cardiomyopathy. Nuclear factor erythroid 2-related factor 2 (Nrf2), a redox-sensing transcription factor, can up-regulate its downstream antioxidant gene expressions in response to oxidative stress. However, the regulatory signal pathway in which high glucose (HG) induces Nrf2 activation is still unclear. Our results demonstrated that HG (33 mM) can indeed stimulate Nrf2 protein expression and translocation into the nucleus in cardiomyocytes, enhancing the downstream antioxidant protein levels. Using siRNAs, p38, JNK, PKCα, and PKCδ, as well as ROS scavengers, it was observed that the dependence of PKCα/PKCδ on ROS production to enhance JNK and p38 phosphorylation mediated HG-induced cardiac Nrf2 expression and activation. Knockdown of Nrf2 by siRNA transfection increased cleaved-caspase3, reduced Bcl2 in the cellular protein level and further exacerbated HG-induced apoptosis. In addition, all of these proteins induced by HG in vitro were also increased in STZ-induced diabetic rat ventricles in vivo. Our study demonstrated that HG-induced cardiac Nrf2 activation occurs through PKCα/PKCδ-ROS-JNK/p38 signaling. These findings may provide a therapeutic target to counteract the oxidative stress associated with diabetic cardiomyopathy. J. Cell. Biochem. 118: 1659-1669, 2017. © 2016 Wiley Periodicals, Inc.

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Personalized medicine in Type 2 Diabetes

Cited by 31 publications

References 53 publications

Cellular apoptosis and cardiac dysfunction in STZ‐induced diabetic rats attenuated by anthocyanins via activation of IGFI‐R/PI3K/Akt survival signaling

Cellular apoptosis and cardiac dysfunction in STZ‐induced diabetic rats attenuated by anthocyanins via activation of IGFI‐R/PI3K/Akt survival signaling

Oolong tea prevents cardiomyocyte loss against hypoxia by attenuating p‐JNK mediated hypertrophy and enhancing P‐IGF1R, p‐akt, and p‐Bad^ser136 activity and by fortifying NRF2 antioxidation system

Nrf2 Activation as a Protective Feedback to Limit Cell Death in High Glucose‐Exposed Cardiomyocytes

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Personalized medicine in Type 2 Diabetes

Cited by 31 publications

References 53 publications

Cellular apoptosis and cardiac dysfunction in STZ‐induced diabetic rats attenuated by anthocyanins via activation of IGFI‐R/PI3K/Akt survival signaling

Cellular apoptosis and cardiac dysfunction in STZ‐induced diabetic rats attenuated by anthocyanins via activation of IGFI‐R/PI3K/Akt survival signaling

Oolong tea prevents cardiomyocyte loss against hypoxia by attenuating p‐JNK mediated hypertrophy and enhancing P‐IGF1R, p‐akt, and p‐Badser136 activity and by fortifying NRF2 antioxidation system

Nrf2 Activation as a Protective Feedback to Limit Cell Death in High Glucose‐Exposed Cardiomyocytes

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Oolong tea prevents cardiomyocyte loss against hypoxia by attenuating p‐JNK mediated hypertrophy and enhancing P‐IGF1R, p‐akt, and p‐Bad^ser136 activity and by fortifying NRF2 antioxidation system