What’s New in Salvage of the Ischemic Myocardium: Estrogen Postconditioning

Babiker, Fawzi; Joseph, Shaji; Juggi, J. S.

doi:10.1159/000330036

Cited by 5 publications

(6 citation statements)

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“…However, a lack of effect on lowering inflammatory cytokines at reperfusion observed in this study could be due to the short period of exposure to DAF or possibly a higher dose is required for that purpose. Previously we reported that lowering TNF-α was essential to protect the heart against I/R injury (Babiker et al 2011;Juggi et al 2011;Babiker et al 2012;Babiker et al 2013), a finding which is now confirmed by this study. Lowering IL-1 and IL-6 levels is associated with reduced heart injury and cardiomyocyte apoptosis (Suzuki et al 2001;Ridker et al 2012;Chen et al 2018).…”

Section: Possible Pathways Of Daf-mediated Heart Protection In This Ssupporting

confidence: 87%

“…(Hulsmans et al 2017;Bajpai et al 2018), an extensive amount of evidence highlights the production of cytokines by cardiomyocytes when stressed for example by hypoxia (Loyer et al 2018). Similar to our findings the cytokines were shown by many studies to contribute to cardiac dysfunction, cardiomyocyte necrosis and apoptosis in I/R injury (Babiker et al 2011;Juggi et al 2011;Babiker et al 2012;Babiker et al 2013). Long-term and short-term treatment with Figure 8.…”

Section: Possible Pathways Of Daf-mediated Heart Protection In This Ssupporting

confidence: 86%

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Micronized flavonoid fraction Daflon 500 protects heart against ischemia–reperfusion injury: an old medicine for a new target

Gouda

Babiker

2020

All Life

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The effects of flavonoids, in the medical formulation Daflon 500 mg (DAF) in protection of the heart against ischemia/reperfusion are not completely understood. Heart function data from Langendorff perfused Wistar rat hearts (n = 8/group) were digitally computed, and the infarct size was evaluated using 2,3,5-triphenyl tetrazolium chloride (TTC) staining and cardiac enzyme levels. The total oxidants (TOS) and antioxidants (TAS) levels as well as pro-and anti-inflammatory cytokines levels were estimated by TOS and TAS assay kits and enzyme-linked immunosorbent assay (ELISA), respectively. The antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT) were evaluated using RAN-DOX kits. Longtime treatment of DAF for 2 or 4 weeks normalized cardiac hemodynamics, vascular dynamics, and heart contractility. A significant reduction in the infarct size and cardiac enzyme levels (P < .05) was produced by DAF treatment. Short time infusion of DAF two hours before inducing ischemia yielded similar results. DAF treatment significantly (P < .05) decreased TOS levels in the perfusion effluent and increased SOD levels in the cardiomyocytes. In conclusion, treatment with DAF prevents the deterioration of cardiac function and ischemic injury caused by oxidative stress and inflammatory cytokines. The protective effects of DAF are possibly due to its antioxidant and anti-inflammatory properties.

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Section: Possible Pathways Of Daf-mediated Heart Protection In This Ssupporting

confidence: 87%

Section: Possible Pathways Of Daf-mediated Heart Protection In This Ssupporting

confidence: 86%

Micronized flavonoid fraction Daflon 500 protects heart against ischemia–reperfusion injury: an old medicine for a new target

Gouda

Babiker

2020

All Life

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“…This study reported an anti-inflammatory effect for Ex-4 and GLP-1 (9-36), as treatment of the heart with these compounds resulted in a significant reduction in TNF-α, IL-1β, and IL-6. Although the presence of immune cells in the isolated heart was unlikely, several studies have shown that I/R causes its damage and cardiac dysfunction to the heart partly by promoting pro-inflammatory cytokine formation [12,42]. Treatment of the rat heart with Ex-4 and GLP-1 (9-36) showed a significant reduction in these pro-inflammatory cytokine protein levels.…”

Section: Discussionmentioning

confidence: 99%

Discrepancy between the Actions of Glucagon-like Peptide-1 Receptor Ligands in the Protection of the Heart against Ischemia Reperfusion Injury

2022

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Tirzepatide is a dual glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) receptor agonist and a promising therapy for type 2 diabetes mellitus (T2DM). GLP-1 is an incretin hormone with therapeutic potential beyond type 2 diabetes mellitus. However, GLP-1 is rapidly degraded by dipeptdyl peptidase-IV (DPP-IV) to GLP-1 (9-36). Exendin-4 (Ex-4) is a DPP-IV-resistant GLP-1 receptor agonist which, when truncated to Ex-4 (9-39), acts as a GLP-1 receptor antagonist. In the present study, hearts isolated from Wistar rats (n = 8 per group) were perfused with a modified Langendorff preparation. Left ventricular (LV) contractility and cardiovascular hemodynamics were evaluated by a data acquisition program and infarct size was evaluated by 2,3,5-Triphenyl-2H-tetrazolium chloride (TTC) staining and cardiac enzyme levels. Hearts were subjected to 30 min regional ischemia, produced by ligation of the left anterior descending (LAD) coronary artery followed by 30 min reperfusion. Hearts were treated during reperfusion with either the non-lipidated precursor of tirzepatide (NLT), GLP-1, GLP-1 (9-36), or Ex-4 in the presence or absence of Ex-4 (9-39). Infusion of GLP-1 (9-36) or Ex-4 protected the heart against I/R injury (p > 0.01) by normalizing cardiac hemodynamic and enzyme levels. Neither GLP-1, NLT, nor Ex-4 (9-39) showed any protection. Interestingly, Ex-4 (9-39) blocked Ex-4-mediated protection but not that of GLP-1 (9-36). These data suggest that Ex-4-mediated protection is GLP-1-receptor-dependent but GLP-1 (9-36)-mediated protection is not.

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“…[18][19][20][21][22] These procedures were proven to attenuate oxidative stress, 20,23 reduce apoptosis and necrosis, 24,25 prevent the opening of mitochondrial permeability transition pore (mPTP) at early phase of reperfusion, 26 save myocytes and normalize heart function. 18,20,22,27,28 Among these procedures, postconditioning provided protection to the myocardium 19 and attenuates apoptosis, necrosis, endothelial dysfunction, ROS formation as well as reperfusion arrhythmias. 29 The application of postconditioning after ischemia and after myocyte injury has occurred, makes it a potentially promising procedure for the clinic that is likely to be preferred by many surgeons compared to other procedures.…”

Section: Introductionmentioning

confidence: 99%

<p>Nanotoxicology of Dendrimers in the Mammalian Heart: ex vivo and in vivo Administration of G6 PAMAM Nanoparticles Impairs Recovery of Cardiac Function Following Ischemia-Reperfusion Injury</p>

Babiker¹,

Benter²,

Akhtar³

2020

IJN

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The effects of polyamidoamine (PAMAM) dendrimers on the mammalian heart are not completely understood. In this study, we have investigated the effects of a sixth-generation cationic dendrimer (G6 PAMAM) on cardiac function in control and diabetic rat hearts following ischemia-reperfusion (I/R) injury. Methods: Isolated hearts from healthy non-diabetic (Ctr) male Wistar rats were subjected to ischemia and reperfusion (I/R). LV contractility and hemodynamics data were computed digitally whereas cardiac damage following I/R injury was assessed by measuring cardiac enzymes. For ex vivo acute exposure experiments, G6 PAMAM was administered during the first 10 mins of reperfusion in Ctr animals. In chronic in vivo studies, nondiabetic rats (Ctr) received either vehicle or daily i.p. injections of G6 PAMAM (40 mg/kg) for 4 weeks. Diabetic (D) animals received either vehicle or daily i.p. injections of G6 PAMAM (10, 20 or 40 mg/kg) for 4 weeks. The impact of G6 PAMAM on pacing-postconditioning (PPC) was also studied in Ctr and D rats. Results: In ex vivo studies, acute administration of G6 PAMAM to isolated Ctr hearts during reperfusion dose-dependently impaired recovery of cardiac hemodynamics and vascular dynamics parameters following I/R injury. Chronic daily i.p. injections of G6 PAMAM significantly (P<0.01) impaired recovery of cardiac function following I/R injury in nondiabetic animals but this was not generally observed in diabetic animals except for CF which was impaired by about 50%. G6 PAMAM treatment completely blocked the protective effects of PPC in the Ctr animals. Conclusion: Acute ex vivo or chronic in vivo treatment with naked G6 PAMAM dendrimer can significantly compromise recovery of non-diabetic hearts from I/R injury and can further negate the beneficial effects of PPC. Our findings are therefore extremely important in the nanotoxicological evaluation of G6 PAMAM dendrimers for potential clinical applications in physiological and pathological settings.

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What’s New in Salvage of the Ischemic Myocardium: Estrogen Postconditioning

Cited by 5 publications

References 4 publications

Micronized flavonoid fraction Daflon 500 protects heart against ischemia–reperfusion injury: an old medicine for a new target

Micronized flavonoid fraction Daflon 500 protects heart against ischemia–reperfusion injury: an old medicine for a new target

Discrepancy between the Actions of Glucagon-like Peptide-1 Receptor Ligands in the Protection of the Heart against Ischemia Reperfusion Injury

<p>Nanotoxicology of Dendrimers in the Mammalian Heart: ex vivo and in vivo Administration of G6 PAMAM Nanoparticles Impairs Recovery of Cardiac Function Following Ischemia-Reperfusion Injury</p>

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