Tanshinone IIA prevents doxorubicin-induced cardiomyocyte apoptosis through Akt-dependent pathway

Hong, Hong Jye; Liu, Ju Chi; Chen, Po‐Yuan; Chen, Jin Jer; Chan, Paul; Cheng, Tzu-Hurng

doi:10.1016/j.ijcard.2010.12.012

Cited by 62 publications

(55 citation statements)

References 15 publications

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“…A kinase which also modulates the PTP is Akt1 [50]. To date a decreased cardiac phosphorylation of the kinase Akt1 (pAkt1) by dox application was not described in the literature but it is known that substances like adiponectin or tanshinone IIA, which reduce the dox mediated cardiac injury, increase the pAkt1 content in the myocardium [51,52]. Admittedly, the regulation of pAkt1 by ERA co-medication correlated only partially with the cardiac function in dox treated mice.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of endothelin receptor A and B inhibitors against doxorubicin-induced cardiomyopathy

Schwebe

Ameling

Hammer

et al. 2015

Biochemical Pharmacology

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Section: Discussionmentioning

confidence: 99%

Protective effects of endothelin receptor A and B inhibitors against doxorubicin-induced cardiomyopathy

Schwebe

Ameling

Hammer

et al. 2015

Biochemical Pharmacology

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“…They all show the properties to protect the heart against cardiac injury (Hong et al, 2012;Ho and Hong, 2011). It is well known that the pharmacologically active compounds of S. miltiorrhiza comprise two fractions: lipophilic diterpenoid tanshinones and water-soluble phenolic acids.…”

Section: Discussionmentioning

confidence: 99%

Cardioprotective effect of Danshensu against myocardial ischemia/reperfusion injury and inhibits apoptosis of H9c2 cardiomyocytes via Akt and ERK1/2 phosphorylation

Yin

Guan

Duan

et al. 2013

European Journal of Pharmacology

135

105

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“…A series of our studies demonstrated tanshinone IIA prevents doxorubicininduced cardiomyocyte apoptosis [2], attenuates H 2 O 2 -induced injury [3]and induces heme oxygenase-1 (HO-1) expression by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway in vascular endothelial cells [4], inhibits angiotensin II-induced cell proliferation via antioxidant activity in rat cardiac fibroblasts [5]. However, the effects and mechanisms of tanshinone IIA on cardio-protection are yet to be delineated.…”

Section: Introductionmentioning

confidence: 87%

Tanshinone IIA Inhibits High Glucose-Induced Collagen Synthesis via Nuclear Factor Erythroid 2-Related Factor 2 in Cardiac Fibroblasts

Tsai

Loh

Lee

et al. 2018

Cell Physiol Biochem

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Background/Aims: Diabetes is associated with increased incidence of myocardial dysfunction, which is partly characterized by interstitial and perivascular fibrosis. Cardiac fibroblasts have been identified as an important participant in the development of cardiac fibrosis. Exposure of cultured cardiac fibroblasts to high glucose resulted in increased collagen synthesis. Tanshinone IIA can alleviate the ventricular fibrosis that develops in a number of different experimental conditions. However, whether tanshinone IIA can prevent high glucose-induced collagen synthesis in cardiac fibroblasts remains unknown. The aim of this study was to evaluate the effects of tanshinone IIA on high glucose-induced collagen synthesis in cardiac fibroblasts. Methods: Rat cardiac fibroblasts were cultured in high glucose (25 mM) media in the absence or presence of tanshinone IIA and the changes in collagen synthesis, transforming growth factor-β1 (TGF-β1) production and related signaling molecules were assessed by ³H-proline incorporation, quantitative polymerase chain reaction, enzyme linked immunosorbent assay, and Western blotting. Results: The results indicate cardiac fibroblasts exposed to high glucose condition show increased cell proliferation and collagen synthesis and these effects were abolished by tanshinone IIA treatment. Furthermore, the inhibitory effect of tanshinone IIA on high glucose induced cell proliferation and collagen synthesis may be associated with its activation of the nuclear factor erythroid 2-related factor 2 (Nrf2) and the inhibition of TGF-β1 production and Smad2/3 phosphorylation. Conclusion: In summary, our results highlights the critical role tanshinone IIA plays as an antioxidant in attenuating high glucose-mediated collagen synthesis through inhibiting TGF-β1/Smad signaling in cardiac fibroblasts which provide a mechanistic basis for the clinical application of tanshinone IIA in the treating diabetic-related cardiac fibrosis.

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Tanshinone IIA prevents doxorubicin-induced cardiomyocyte apoptosis through Akt-dependent pathway

Cited by 62 publications

References 15 publications

Protective effects of endothelin receptor A and B inhibitors against doxorubicin-induced cardiomyopathy

Protective effects of endothelin receptor A and B inhibitors against doxorubicin-induced cardiomyopathy

Cardioprotective effect of Danshensu against myocardial ischemia/reperfusion injury and inhibits apoptosis of H9c2 cardiomyocytes via Akt and ERK1/2 phosphorylation

Tanshinone IIA Inhibits High Glucose-Induced Collagen Synthesis via Nuclear Factor Erythroid 2-Related Factor 2 in Cardiac Fibroblasts

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