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Curcumin Downregulates Phosphate Carrier and Protects against Doxorubicin Induced Cardiomyocyte Apoptosis.

Junkun L, Erfu C, Tony H, Xin L, Sudeep KC, Mingliang Z, Yanqin W, XiangQian Q - Biomed Res Int (2016)

Bottom Line: Results.Interestingly, the effect was not clearly dose dependent and the concentration of 12 mg/L was more efficient than 15 and 10 mg/L.Conclusion.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology Division II, Tianjin Medical University Cardiovascular Institute, TEDA International Cardiovascular Hospital, Tianjin 300070, China; Department of Cardiology Division II, Jiamusi University, 1st Affiliated Hospital, Jiamusi, Heilongjiang 154003, China.

ABSTRACT
Aim. To explore the effects of curcumin on phosphate carrier (PiC) and its role in protection against doxorubicin induced myocyte toxicity. Methods. Using H9c2 cell line, the cardiotoxic effect of doxorubicin and its mitigation by curcumin were studied. H9c2 cells were cultured with doxorubicin and/or curcumin at various concentrations. Analysis for apoptosis of H9c2 was done using flow cytometry. Confocal laser scanning microscopy was used to record the fluorescence intensity ratios and to determine the mitochondrial permeability transition pore (MPTP) opening state. Oxidative stress was measured using glutathione level, superoxide dismutase activities, and malondialdehyde content. The effect of doxorubicin and curcumin on PiC gene expression was measured by real-time PCR. Results. Curcumin decreased mRNA of PiC and was partly protective against oxidative stress, loss of mitochondrial transmembrane potential, and apoptosis induced by doxorubicin. Interestingly, the effect was not clearly dose dependent and the concentration of 12 mg/L was more efficient than 15 and 10 mg/L. Conclusion. Curcumin downregulates PiC and partly protects against doxorubicin induced oxidative stress and myocyte apoptosis.

No MeSH data available.


Related in: MedlinePlus

Oxidative stress showed obvious increase with time after addition of doxorubicin and this was alleviated by curcumin. (#P < 0.05 versus Negative control (Dox 0 h-Cur 0 min)) (∗P < 0.05 versus Cur 0, Dox + at each time point). (a) Following culture with doxorubicin, GSH levels declined with time while curcumin obviated this effect at various doses. (b) SOD activity decreased with time after culture with doxorubicin, and this effect was decreased by curcumin at various doses. (c) Doxorubicin culture increased MDA content over time, an effect that was attenuated by curcumin. 12 mg/L was the most efficient dose of curcumin in decreasing MDA content following culture with doxorubicin.
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fig1: Oxidative stress showed obvious increase with time after addition of doxorubicin and this was alleviated by curcumin. (#P < 0.05 versus Negative control (Dox 0 h-Cur 0 min)) (∗P < 0.05 versus Cur 0, Dox + at each time point). (a) Following culture with doxorubicin, GSH levels declined with time while curcumin obviated this effect at various doses. (b) SOD activity decreased with time after culture with doxorubicin, and this effect was decreased by curcumin at various doses. (c) Doxorubicin culture increased MDA content over time, an effect that was attenuated by curcumin. 12 mg/L was the most efficient dose of curcumin in decreasing MDA content following culture with doxorubicin.

Mentions: In order to measure oxidative stress induced by doxorubicin in H9c2 cells, we used 3 kits. As anticipated, with increased time of cell culturing with doxorubicin, there was a marked increase in oxidative stress as shown by GSH levels decline, MDA content increase, and SOD activities decrease. The oxidative stress progressively reduced with addition of increasing amounts of curcumin. 12 mg/L dose of curcumin showed the most obvious decline. These results suggest that curcumin partly protects against high oxidative stress states caused by doxorubicin (Figure 1).


Curcumin Downregulates Phosphate Carrier and Protects against Doxorubicin Induced Cardiomyocyte Apoptosis.

Junkun L, Erfu C, Tony H, Xin L, Sudeep KC, Mingliang Z, Yanqin W, XiangQian Q - Biomed Res Int (2016)

Oxidative stress showed obvious increase with time after addition of doxorubicin and this was alleviated by curcumin. (#P < 0.05 versus Negative control (Dox 0 h-Cur 0 min)) (∗P < 0.05 versus Cur 0, Dox + at each time point). (a) Following culture with doxorubicin, GSH levels declined with time while curcumin obviated this effect at various doses. (b) SOD activity decreased with time after culture with doxorubicin, and this effect was decreased by curcumin at various doses. (c) Doxorubicin culture increased MDA content over time, an effect that was attenuated by curcumin. 12 mg/L was the most efficient dose of curcumin in decreasing MDA content following culture with doxorubicin.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4835619&req=5

fig1: Oxidative stress showed obvious increase with time after addition of doxorubicin and this was alleviated by curcumin. (#P < 0.05 versus Negative control (Dox 0 h-Cur 0 min)) (∗P < 0.05 versus Cur 0, Dox + at each time point). (a) Following culture with doxorubicin, GSH levels declined with time while curcumin obviated this effect at various doses. (b) SOD activity decreased with time after culture with doxorubicin, and this effect was decreased by curcumin at various doses. (c) Doxorubicin culture increased MDA content over time, an effect that was attenuated by curcumin. 12 mg/L was the most efficient dose of curcumin in decreasing MDA content following culture with doxorubicin.
Mentions: In order to measure oxidative stress induced by doxorubicin in H9c2 cells, we used 3 kits. As anticipated, with increased time of cell culturing with doxorubicin, there was a marked increase in oxidative stress as shown by GSH levels decline, MDA content increase, and SOD activities decrease. The oxidative stress progressively reduced with addition of increasing amounts of curcumin. 12 mg/L dose of curcumin showed the most obvious decline. These results suggest that curcumin partly protects against high oxidative stress states caused by doxorubicin (Figure 1).

Bottom Line: Results.Interestingly, the effect was not clearly dose dependent and the concentration of 12 mg/L was more efficient than 15 and 10 mg/L.Conclusion.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology Division II, Tianjin Medical University Cardiovascular Institute, TEDA International Cardiovascular Hospital, Tianjin 300070, China; Department of Cardiology Division II, Jiamusi University, 1st Affiliated Hospital, Jiamusi, Heilongjiang 154003, China.

ABSTRACT
Aim. To explore the effects of curcumin on phosphate carrier (PiC) and its role in protection against doxorubicin induced myocyte toxicity. Methods. Using H9c2 cell line, the cardiotoxic effect of doxorubicin and its mitigation by curcumin were studied. H9c2 cells were cultured with doxorubicin and/or curcumin at various concentrations. Analysis for apoptosis of H9c2 was done using flow cytometry. Confocal laser scanning microscopy was used to record the fluorescence intensity ratios and to determine the mitochondrial permeability transition pore (MPTP) opening state. Oxidative stress was measured using glutathione level, superoxide dismutase activities, and malondialdehyde content. The effect of doxorubicin and curcumin on PiC gene expression was measured by real-time PCR. Results. Curcumin decreased mRNA of PiC and was partly protective against oxidative stress, loss of mitochondrial transmembrane potential, and apoptosis induced by doxorubicin. Interestingly, the effect was not clearly dose dependent and the concentration of 12 mg/L was more efficient than 15 and 10 mg/L. Conclusion. Curcumin downregulates PiC and partly protects against doxorubicin induced oxidative stress and myocyte apoptosis.

No MeSH data available.


Related in: MedlinePlus