Protection against acute adriamycin-induced cardiotoxicity by garlic: Role of endogenous antioxidants and inhibition of TNF-α expression

Mukherjee, Sumanta; Banerjee, Sanjay K.; Maulik, Mohua; Dinda, Amit Kumar; Kk, Talwar; Maulik, Subir Kumar

doi:10.1186/1471-2210-3-16

Cited by 130 publications

(20 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Studies have confirmed that DOX-derived ROS could act as an intrinsic stress that activates mitogen activated protein kinases (MAPK), p38, JNK, and NF- κ B pathways as well as intracellular p53 accumulation, leading to an increase in proinflammatory cytokines (TNF- α and IL-1 β ) and alteration in the ratio of proapoptotic proteins to antiapoptotic proteins (e.g., Bax to Bcl-2), cytochrome C (Cyto C) release, and caspase-3 (C3) activation [22–24]. The present study aims to investigate the potential anti-inflammation and antiapoptosis effect of hydrogen-rich saline on DOX-induced cardiotoxicity and hepatotoxicity in Wistar albino rats.…”

Section: Introductionmentioning

confidence: 99%

Hydrogen-Rich Saline Attenuates Cardiac and Hepatic Injury in Doxorubicin Rat Model by Inhibiting Inflammation and Apoptosis

Gao

Yang

Fan

et al. 2016

Mediators of Inflammation

View full text Add to dashboard Cite

Doxorubicin (DOX) remains the most effective anticancer agent which is widely used in several adult and pediatric cancers, but its application is limited for its cardiotoxicity and hepatotoxicity. Hydrogen, as a selective antioxidant, is a promising potential therapeutic option for many diseases. In this study, we found that intraperitoneal injection of hydrogen-rich saline (H2 saline) ameliorated the mortality, cardiac dysfunction, and histopathological changes caused by DOX in rats. Meanwhile, serum brain natriuretic peptide (BNP), aspartate transaminase (AST), alanine transaminase (ALT), albumin (ALB), tissue reactive oxygen species (ROS), and malondialdehyde (MDA) levels were also attenuated after H2 saline treatment. What is more, we further demonstrated that H2 saline treatment could inhibit cardiac and hepatic inflammation and apoptosis relative proteins expressions by western blotting test. In conclusion, our results revealed a protective effect of H2 saline on DOX-induced cardiotoxicity and hepatotoxicity in rats by inhibiting inflammation and apoptosis.

show abstract

Section: Introductionmentioning

confidence: 99%

Hydrogen-Rich Saline Attenuates Cardiac and Hepatic Injury in Doxorubicin Rat Model by Inhibiting Inflammation and Apoptosis

Gao

Yang

Fan

et al. 2016

Mediators of Inflammation

View full text Add to dashboard Cite

show abstract

“…However, its practical therapeutic use is limited by the development of dose-dependent chronic cardiomyopathy [3, 4]. Previous studies on the mechanisms of ADR cardiotoxicity have reported that the formation of free reactive oxygen radicals [5, 6], release of cardiotoxic cytokines [7, 8], cytoskeletal changes [9] and intracellular calcium overload [10, 11] might be involved in the mechanisms of ADR cardiotoxicity. In our study, we found that ADR induces a higher rate of reactive oxygen species formation with depression of antioxidant enzyme activities and a decrease in total antioxidant capability.…”

Section: Discussionmentioning

confidence: 99%

Effects of Pyrrolidine Dithiocarbamate on Antioxidant Enzymes in Cardiomyopathy Induced by Adriamycin in Rats

Liu²,

Li³

et al. 2008

Cardiology

View full text Add to dashboard Cite

Objective: The clinical usefulness of adriamycin (ADR) is restricted by the frequent induction of dose-dependent chronic cardiomyopathy. Previous studies on ADR cardiotoxicity have reported that the formation of free reactive oxygen radicals might be involved in ADR cardiotoxicity. Pyrrolidine dithiocarbamate (PDTC) is a potent antioxidant in vivo and in vitro. The present study was undertaken to examine the effects of PDTC on antioxidant enzymes in cardiomyopathy induced by ADR in rats. Methods: Thirty-two male Wistar rats were randomly divided into 4 groups: control, ADR, PDTC, and ADR+PDTC. After 30 days, myocardial histopathological and electron microscopic examinations were performed: the myocardial content of superoxide anion and lipid peroxides were examined; the myocardial total antioxygenation capability (T-AOC) and activity of glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) were examined; myocardial GSH-Px, Mn-SOD and Cu,Zn-SOD gene expressions were examined by RT-PCR analysis, and the myocardial expression of GSH-Px, Mn-SOD and Cu,Zn-SOD proteins was assessed by Western blot analysis. Results: At 30 days, ADR-induced cardiomyopathy was confirmed by structural examination. The changes were prevented by PDTC. Myocardial superoxide anion and lipid peroxides were increased by ADR, and these changes were also inhibited by PDTC. ADR decreased myocardial T-AOC and the activity of GSH-Px and SOD, and these changes were likewise inhibited by PDTC. mRNA and protein expression of GSH-Px and Mn-SOD were depressed by ADR treatment and prevented by PDTC. Cu,Zn-SOD mRNA and protein levels were not significantly changed by ADR or PDTC. Conclusion: PDTC prevented ADR cardiomyopathy in rats by upregulating GSH-Px and SOD activation, which is associated with changes in the expression of GSH-Px and Mn-SOD transcript and protein levels.

show abstract

“…Chronically, doxorubicin can increase TNF-α [47] and IL-1 [48] gene expression in rats. However, in this study myocardial TNF-α levels did not change after doxorubicin administration.…”

Section: Discussionmentioning

confidence: 99%

Acute Doxorubicin-Induced Cardiotoxicity is Associated with Matrix Metalloproteinase-2 Alterations in Rats

Polegato

Minicucci

Azevedo

et al. 2015

Cell Physiol Biochem

View full text Add to dashboard Cite

Background: Doxorubicin can cause cardiotoxicity. Matrix metalloproteinases (MMP) are responsible for degrading extracellular matrix components which play a role in ventricular dilation. Increased MMP activity occurs after chronic doxorubicin treatment. In this study we evaluated in vivo and in vitro cardiac function in rats with acute doxorubicin treatment, and examined myocardial MMP and inflammatory activation, and gene expression of proteins involved in myocyte calcium transients. Methods: Wistar rats were injected with doxorubicin (Doxo, 20 mg/kg) or saline (Control). Echocardiogram was performed 48 h after treatment. Myocardial function was assessed in vitro in Langendorff preparation. Results: In left ventricle, doxorubicin impaired fractional shortening (Control 0.59±0.07; Doxo 0.51±0.05; p<0.001), and increased isovolumetric relaxation time (Control 20.3±4.3; Doxo 24.7±4.2 ms; p=0.007) and myocardial passive stiffness. MMP-2 activity, evaluated by zymography, was increased in Doxo (Control 141338 ± 8924; Doxo 188874 ± 7652 arbitrary units; p<0.001). There were no changes in TNF-α, INF-γ, IL-10, and ICAM-1 myocardial levels. Expression of phospholamban, Serca-2a, and ryanodine receptor did not differ between groups. Conclusion: Acute doxorubicin administration induces in vivo left ventricular dysfunction and in vitro increased myocardial passive stiffness in rats. Cardiac dysfunction is related to myocardial MMP-2 activation. Increased inflammatory stimulation or changed expression of the proteins involved in intracellular calcium transients is not involved in acute cardiac dysfunction.

show abstract

Protection against acute adriamycin-induced cardiotoxicity by garlic: Role of endogenous antioxidants and inhibition of TNF-α expression

Cited by 130 publications

References 29 publications

Hydrogen-Rich Saline Attenuates Cardiac and Hepatic Injury in Doxorubicin Rat Model by Inhibiting Inflammation and Apoptosis

Hydrogen-Rich Saline Attenuates Cardiac and Hepatic Injury in Doxorubicin Rat Model by Inhibiting Inflammation and Apoptosis

Effects of Pyrrolidine Dithiocarbamate on Antioxidant Enzymes in Cardiomyopathy Induced by Adriamycin in Rats

Acute Doxorubicin-Induced Cardiotoxicity is Associated with Matrix Metalloproteinase-2 Alterations in Rats

Contact Info

Product

Resources

About