Pentoxifylline Prevents Driamycin-Induced Myocardial Fibrosis and Apoptosis in Rats

Zang, Zhijun; Li, Shujuan; Lin, Yuese; Li, Xuandi; Li, Yunquan; Qin, Youzhen; Wang, Huishen; Jiang, Manli; Zhu, Ling

doi:10.1536/ihj.15-203

Cited by 9 publications

(6 citation statements)

References 33 publications

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“…Similar to the report of Zang,29) during the experiment, myocardium injury induced by DOX treatment were aggravated in mice, but there were no signs of over-toxicity or deaths that happened. M-mode image of the LV displays the ventricular walls, LV cavity, and cardiac function measurements (Figure 1A).…”

Section: Echocardiography and Histologic Analysis After Dcmsupporting

confidence: 84%

Cardiac Nestin<sup>+</sup> Cells Derived from Early Stage of Dilated Cardiomyopathy Enhanced the Survival of the Doxorubicin-Injured Cardiac Muscle HL-1 Cells

Xie

Liao

et al. 2018

Int. Heart J.

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SummaryDilated cardiomyopathy (DCM), as one of the common cardiomyopathies, is a disease of the heart muscle; however, the etiology and pathogenesis of DCM were still poorly understood. Nestin has been reported a special marker of stem/progenitor cells in various tissues, and the tissue resident Nestin + cells could promote the wound healing and tissue remodeling. However, it remains unclear whether Nestin + cells participate in the protection of cardiomyocytes during the pathogenesis of DCM. Here the model of mice DCM was induced by doxorubicin (DOX) intraperitoneal injection and observed heart failure and ventricular enlargement via echocardiography and histologic analysis, respectively. During DCM pathogenesis, the number of Nestin + cells showed a significant peak on day 6 after DOX treatment, which then gradually decreases to lower than normal levels after day 30 in the total population of the heart. Furthermore, we found that the isolated increased heart-derived Nestin + cells are mesenchymal property and could protect DOX-induced HL-1 cells toxicity in vitro by promoting their proliferation and inhibiting their apoptosis. Collectively, our results showed that Nestin + cells increased during DCM pathogenesis and played an important role in protecting against the DOX-induced HL-1 cells loss via regulating proliferation and apoptosis. Thus, the loss of Nestin + cells might be an etiology to DCM pathogenesis, and these cells could be a promising candidate cell source for study and treatment of DCM patients.(Int Heart J 2018; 59: 180-189)

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Section: Echocardiography and Histologic Analysis After Dcmsupporting

confidence: 84%

Cardiac Nestin<sup>+</sup> Cells Derived from Early Stage of Dilated Cardiomyopathy Enhanced the Survival of the Doxorubicin-Injured Cardiac Muscle HL-1 Cells

Xie

Liao

et al. 2018

Int. Heart J.

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“…For instance, PX administration inhibits myocardial apoptosis after adriamycin-induced dilated cardiomyopathy, by blocking the caspase-3 dependent apoptotic pathway. 33 However, in our study, it did not influence these parameters.…”

Section: Discussioncontrasting

confidence: 72%

Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure

Minicucci

Oliveira

Santos

et al. 2016

Arquivos Brasileiros De Cardiologia

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BackgroundTobacco smoke exposure is an important risk factor for cardiac remodeling. Under this condition, inflammation, oxidative stress, energy metabolism abnormalities, apoptosis, and hypertrophy are present. Pentoxifylline has anti‑inflammatory, anti-apoptotic, anti-thrombotic and anti-proliferative properties.ObjectiveThe present study tested the hypothesis that pentoxifylline would attenuate cardiac remodeling induced by smoking.MethodsWistar rats were distributed in four groups: Control (C), Pentoxifylline (PX), Tobacco Smoke (TS), and PX-TS. After two months, echocardiography, invasive blood pressure measurement, biochemical, and histological studies were performed. The groups were compared by two-way ANOVA with a significance level of 5%.ResultsTS increased left atrium diameter and area, which was attenuated by PX. In the isolated heart study, TS lowered the positive derivate (+dp/dt), and this was attenuated by PX. The antioxidants enzyme superoxide dismutase and glutathione peroxidase were decreased in the TS group; PX recovered these activities. TS increased lactate dehydrogenase (LDH) and decreased 3-hydroxyacyl Coenzyme A dehydrogenases (OH-DHA) and citrate synthase (CS). PX attenuated LDH, 3-OH-DHA and CS alterations in TS-PX group. TS increased IL-10, ICAM-1, and caspase-3. PX did not influence these variables.ConclusionTS induced cardiac remodeling, associated with increased inflammation, oxidative stress, apoptosis, and changed energy metabolism. PX attenuated cardiac remodeling by reducing oxidative stress and improving cardiac bioenergetics, but did not act upon cardiac cytokines and apoptosis.

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“…Immunohistochemistry: At the end of reperfusion, the heart was sectioned and small pieces of the heart were immersion fixed for 24 hours in 10% formalin solution. 16) Next, all of the samples were processed using a standard histological procedure. 12) After blocking in 5% BSA for 30 minutes, sections were incubated with anti-Sirt1 antibody (1:200) and anti-PGC-1α antibody (1:300) at 4°C overnight.…”

Section: Analysis Of Mda Atp and Sod Levels In Myocardial Tissuementioning

confidence: 99%

Exogenous Hydrogen Sulﬁde Postconditioning Protects Isolated Rat Hearts From Ischemia/Reperfusion Injury Through Sirt1/PGC-1α Signaling Pathway

Zhou

Mao

et al. 2016

Int. Heart J.

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Sirt1 is a highly conserved nicotinamide adenine dinucleotide (NAD(+)) dependent histone deacetylase which plays an important role in heart diseases. Studies performed with Sirt1 activators indicated that it protects cells from ischemia/ reperfusion (I/R) injury. The protective effects of H2S against I/R injury also have been recognized. Hence, the present study was designed to explore whether Sirt1/PGC-1α participates in the protection of exogenous H2S postconditioning against I/R injury in isolated rat hearts. Isolated rat hearts were subjected to 30 minutes of global ischemia followed by 60 minutes of reperfusion after 20 minutes of equilibrium. During this procedure, the hearts were exposed to NaHS (10 μmol/L) treatment in the absence or presence of the selective Sirt1 inhibitor EX-527 (10 μmol/L). NaHS exerted a protective effect on isolated rat hearts subjected to I/R, as shown by the improved expression of Sirt1/PGC-1α associated with restoration of Sirt1 nuclear localization, cardiac function, decreased myocardial infarct size, decreased myocardial enzyme release, and several biochemical parameters, including up-regulation of the ATP and SOD levels, and down-regulation of the MDA level. However, treatment with EX-527 could partially prevent the above effects of NaHS postconditioning. These results indicate that H2S confers protective effects against I/R injury through the activation of Sirt1/PGC1α.

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Pentoxifylline Prevents Driamycin-Induced Myocardial Fibrosis and Apoptosis in Rats

Cited by 9 publications

References 33 publications

Cardiac Nestin<sup>+</sup> Cells Derived from Early Stage of Dilated Cardiomyopathy Enhanced the Survival of the Doxorubicin-Injured Cardiac Muscle HL-1 Cells

Cardiac Nestin<sup>+</sup> Cells Derived from Early Stage of Dilated Cardiomyopathy Enhanced the Survival of the Doxorubicin-Injured Cardiac Muscle HL-1 Cells

Pentoxifylline Attenuates Cardiac Remodeling Induced by Tobacco Smoke Exposure

Exogenous Hydrogen Sulﬁde Postconditioning Protects Isolated Rat Hearts From Ischemia/Reperfusion Injury Through Sirt1/PGC-1α Signaling Pathway

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