The modulatory effect of lithium on doxorubicin-induced cardiotoxicity in rat

Rahimi-Balaei, Maryam; Momeny, Majid; Babaeikelishomi, Rohollah; Mehr, Shahram Ejtemaei; Tavangar, Seyed Mohammad; Dehpour, Ahmad Reza

doi:10.1016/j.ejphar.2010.05.046

Cited by 26 publications

(11 citation statements)

References 44 publications

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“…Similar results were obtained by previous studies [Richard et al, 2011;Colak et al, 2012;Warpe et al, 2015]. ECG revealed significant prolongation of QT interval in DOX-administered groups (II, III) as reported by Rahimi_Balaei et al [2010]; Ashour et al [2011] and Warpe et al [2015]; denoting delayed repolarization and a negative chronotropic effect [Gandhi et al, 2013] or metabolic and electrolyte abnormalities associated with developed heart failure [Hunter et al, 2008].…”

Section: Discussionsupporting

confidence: 88%

Functional and Structural Assessment of the Effect of Human Umbilical Cord Blood Mesenchymal Stem Cells in Doxorubicin‐Induced Cardiotoxicity

Allah

Hussein

Hasan

et al. 2017

J of Cellular Biochemistry

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Cardiomyopathy induced by doxorubicin (DOX) was recognized at an early stage and also several years after drug administration. Mesenchymal stem cells (MSCs) have many properties that make them suitable for preventive and/or regenerative therapies. In this study, we evaluated the effect of MSCs in the functional and the structural improvement of DOX-induced cardiomyopathy in rats. Ninety adult male albino rats were randomly divided into three equal groups of thirty rats each: Group I (control): rats received normal saline. Group II (DOX- group): rats received DOX. Group III (DOX-MSCs group): rats received DOX for 2 weeks then human umbilical cord blood mesenchymal stem cells (hUCB-MSCs). Rats in all groups were evaluated for: physical condition, electrocardiography (ECG), and hemodynamic parameters. Serum cardiac troponin I (cTnI), malondialdehyde (MDA), total antioxidant capacity (TAC), and DNA fragmentation on heart tissue isolated DNA were estimated for evaluation of the mechanism and the extent of the damage. Hearts were examined histopathologically for detection of MSCs homing, structural evaluation, with counting of the collagen fibers for evaluation of fibrosis. DOX-administered rats showed significant functional and structural deterioration. DOX-MSCs treated rats (group III) showed improved functional and structural criteria with restoration of all biochemical indicators of cardiac damage and reactive oxygen species (ROS) to normal, as well. In Conclusion, hUCB-MSCs significantly ameliorated the cardiotoxic manifestations as shown by biochemical, functional, and structural cardiac improvement. J. Cell. Biochem. 118: 3119-3129, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Discussionsupporting

confidence: 88%

Functional and Structural Assessment of the Effect of Human Umbilical Cord Blood Mesenchymal Stem Cells in Doxorubicin‐Induced Cardiotoxicity

Allah

Hussein

Hasan

et al. 2017

J of Cellular Biochemistry

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“…Lithium is used for the treatment of bipolar disorder, via the inhibition of glycogen synthase kinase-3β enzyme (GSK-3β) (Lenox andHahn, 2000, Phiel andKlein, 2001). Many clinical and experimental studies showed that lithium from ranges 10 to 400 mg/kg caused neuroprotection in different conditions (Boyko et al, 2015, Chrislip et al, 1984, Dhawan et al, 1999, Frey et al, 2006, Hajek and Weiner, 2016, Khairova et al, 2012, Machado-Vieira et al, 2009, Rahimi et al, 2014, Rahimi_Balaei et al, 2010. Several clinical reviews showed that optimum lithium concentration after therapeutic doses is 0.6-0.75 mmol/L.…”

Section: Introductionmentioning

confidence: 95%

“…The selection of doses of MPH was done according to previous work results on neurodegenerative doses of MPH in animal models and human subjects (Balcioglu, Ren, 2009, Gerasimov, Franceschi, 2000, Hannestad, Gallezot, 2010, Motaghinejad, Motevalian, 2015e, Quinn, Wigal, 2004, Schiffer, Volkow, 2006, Teo, Stirling, 2002, Thanos, Robison, 2015, Volkow, Wang, 2001, Wargin, Patrick, 1983, and neuroprotective doses of lithium was obtained from previous work on human and animal studies (Boyko, Nassar, 2015, Chrislip, Anger, 1984, Dhawan, Singh, 1999, Frey, Valvassori, 2006, Hajek and Weiner, 2016, Khairova, Pawar, 2012, Machado-Vieira, Manji, 2009, Rahimi, Dehpour, 2014, Rahimi_Balaei, Momeny, 2010. There are several references in relation to clinical relevance of choosing MPH and lithium doses in our experiment, and also the relationship that exist between doses and plasma levels in experimental subjects (Balcioglu, Ren, 2009, Hanak, Chevillard, 2014, Morrison, Pritchard, 1971, Severus, Kleindienst, 2007, Severus, Kleindienst, 2008, Teo, Stirling, 2002, Thanos, Robison, 2015, Wargin, Patrick, 1983 Elevated Plus Maze (EPM) was used to assess anxiety in animal models.…”

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confidence: 99%

The neuroprotective effect of lithium against high dose methylphenidate: Possible role of BDNF

et al. 2016

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“…Iron may catalyse ROS formation in Dox-induced cardiotoxicity 4 , 5 , and DEX may chelate iron before it catalyses the conversion of O 2 •− and H 2 O 2 to more damaging oxidants 25 . According to previous studies 26 – 28 , we established a rat model of cumulative cardiotoxicity, Dox and Dox combined with DEX were given for 4 or 8 weeks, respectively. Detections of plasma cTnT and Ca-Mg-ATP revealed that significant cardiotoxicity was achieved after 4-week and 8-week Dox treatment, but DEX could efficiently alleviate Dox-induced cardiac damage.…”

Section: Discussionmentioning

confidence: 99%

Activation of miR-34a-5p/Sirt1/p66shc pathway contributes to doxorubicin-induced cardiotoxicity

Zhu

Zhi-qin

et al. 2017

Sci Rep

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The molecular mechanisms underlying anthracyclines-induced cardiotoxicity have not been well elucidated. MiRNAs were revealed dysregulated in the myocardium and plasma of rats received Dox treatment. MicroRNA-34a-5p (miR-34a-5p) was verified increased in the myocardium and plasma of Dox-treated rats, but was reversed in rats received Dox plus DEX treatments. Human miR-34a-5p was also observed increased in the plasma of patients with diffuse large B-cell lymphoma after 9- and 16-week epirubicin therapy. Up-regulation of miR-34a-5p was observed in Dox-induced rat cardiomyocyte H9c2 cells. MiR-34a-5p could augment Bax expression, but inhibited Bcl-2 expression, along with the increases of the activated caspase-3 and mitochondrial potentials in H9C2 cells. MiR-34a-5p was verified to modulate Sirt1 expression post-transcriptionally. In parallel to Sirt1 siRNA, miR-34a-5p could enhance p66shc expression, accompanied by increases of Bax and the activated caspase-3 and a decrease of Bcl-2 in H9c2 cells. Moreover, enforced expression of Sirt1 alleviated Dox-induced apoptosis of H9c2 cells, with suppressing levels of p66shc, Bax, the activated caspase-3 and miR-34a-5p, and enhancing Bcl-2 expression. Therefore, miR-34a-5p enhances cardiomyocyte apoptosis by targeting Sirt1, activation of miR-34a-5p/Sirt1/p66shc pathway contributes to Dox-induced cardiotoxicity, and blockage of this pathway represents a potential cardioprotective effect against anthracyclines.

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The modulatory effect of lithium on doxorubicin-induced cardiotoxicity in rat

Cited by 26 publications

References 44 publications

Functional and Structural Assessment of the Effect of Human Umbilical Cord Blood Mesenchymal Stem Cells in Doxorubicin‐Induced Cardiotoxicity

Functional and Structural Assessment of the Effect of Human Umbilical Cord Blood Mesenchymal Stem Cells in Doxorubicin‐Induced Cardiotoxicity

The neuroprotective effect of lithium against high dose methylphenidate: Possible role of BDNF

Activation of miR-34a-5p/Sirt1/p66shc pathway contributes to doxorubicin-induced cardiotoxicity

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