Paradoxical effect of testosterone supplementation therapy on cardiac ischemia/reperfusion injury in aged rats

Seara, Fernando A.C.; Barbosa, Raiana Andrade Quintanilha; Santos, Marcus Vinícius N; Domingos, Ainá E.; Monnerat, Gustavo; Carvalho, Adriana Bastos; Olivares, Emerson Lopes; Mill, José Geraldo; Nascimento, José; Carvalho, Antônio Carlos Campos de

doi:10.1016/j.jsbmb.2019.03.012

Cited by 8 publications

(2 citation statements)

References 51 publications

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“…Intravenous administration of DEX before cardiopulmonary bypass can attenuate the cardiovascular response d, 4 d, 7 d and 14 d after induction [19] . Studies have shown that when vitamin C induces Embryonic stem cells (Es) to differentiate into cardiomyocytes, β-MHC gene expression is also present before induction, and the expression gradually increases after induction, reaching the peak at 10 d, and then gradually decreases [20] . After the interference of titin gene expression, the distribution of β-MHC was dispersed, and the expression of the β-MHC gene did not alter considerably from before the interference, and the arrangement of myofibrils was disordered [21] .…”

Section: Resultsmentioning

confidence: 99%

Protective Effect and Mechanism of Dexmedetomidine on Myocardial Ischemia-Reperfusion Injury by Regulating Titin/Myosin Heavy Chain Signal Axis

Lei

2023

IJPS

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To examine the protective impact of dexmedetomidine on myocardial ischemia-reperfusion injury, and to clarify the relationship between dexmedetomidine and titin/myosin heavy chain signal axis. Rat cardiac H9c2 cells were purchased as the research object. They were divided into three groups; blank control group, hypoxia concentration incubation group (hypoxia group) and dexmedetomidine group. The lactate dehydrogenase, cardiac troponin I and creatine kinase-myocardial band in myocardial cells of rats in hypoxia group were higher than the blank control group. The lactate dehydrogenase, cardiac troponin I and creatine kinase-myocardial band in myocardial cells of rats in differentially expressed gene were reduced than hypoxia group. Compared with the control group, in the hypoxia group, there was no discernible variation in the level of telomerase in cardiomyocytes. The telomerase level of cardiomyocytes in the differentially expressed gene was higher than the hypoxia group. Compared with the control group, the titin protein in myocardial cells of hypoxia group was decreased, the beta-myosin heavy chain protein was increased while the level of titin in cardiac myocytes of differentially expressed gene was higher than that of hypoxia group, and the beta-myosin heavy chain was reduced than hypoxia group. Compared with the blank control group, the phospho-extracellular signal regulated kinases protein in cardiac myocytes of rats in hypoxia group and differentially expressed gene was lower, and the nuclear factor kappa B protein was higher. However, the phospho-extracellular signal regulated kinases protein in cardiac myocytes of rats in differentially expressed gene was higher than in hypoxia group and the nuclear factor kappa B was reduced than hypoxia group. The phospho-phosphatidylinositol-3 kinase and phospho-protein kinase B in cardiac myocytes of rats in hypoxia group and differentially expressed gene were higher than the blank control group, and the phospho-phosphatidylinositol-3 kinase and phospho-protein kinase B in rats in differentially expressed gene were higher than hypoxia group. The protective effect of dexmedetomidine on myocardial ischemia-reperfusion injury may be related to reducing cardiomyocyte apoptosis and inhibiting titin differentially expressed gene radiation by activating extracellular signal regulated kinases 1/2 and phosphatidylinositol-3 kinase signaling pathways.

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Section: Resultsmentioning

confidence: 99%

Protective Effect and Mechanism of Dexmedetomidine on Myocardial Ischemia-Reperfusion Injury by Regulating Titin/Myosin Heavy Chain Signal Axis

Lei

2023

IJPS

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“…In contrast, other studies showed that infarct size, contractility, and mitochondrial function were impaired in castrated rats upon IRI compared with gonad-intact rats and that testosterone replacement attenuated these impairments [ 61 ]. Interestingly, testosterone treatment improved cardiac contractile function and reduced the infarct size in a more pronounced manner in aged male rats, while having no effects on the hearts of young adult rats, indicating a role of aging [ 62 ]. These conflicting experimental reports reflect clinical data wherein patients with prostate cancer undergoing androgen deprivation therapy exhibited enhanced incident MI and shorter times to fatal MI, while other studies showed no significant effects of androgen deprivation therapy [ 63 ].…”

Section: Pathophysiological Sex Differences In Myocardial Irimentioning

confidence: 99%

Sex Differences in Therapies against Myocardial Ischemia-Reperfusion Injury: From Basic Science to Clinical Perspectives

Medzikovic,

Azem,

Sun

et al. 2023

Cells

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Mortality from myocardial infarction (MI) has declined over recent decades, which could be attributed in large part to improved treatment methods. Early reperfusion is the cornerstone of current MI treatment. However, reoxygenation via restored blood flow induces further damage to the myocardium, leading to ischemia-reperfusion injury (IRI). While experimental studies overwhelmingly demonstrate that females experience greater functional recovery from MI and decreased severity in the underlying pathophysiological mechanisms, the outcomes of MI with subsequent reperfusion therapy, which is the clinical correlate of myocardial IRI, are generally poorer for women compared with men. Distressingly, women are also reported to benefit less from current guideline-based therapies compared with men. These seemingly contradicting outcomes between experimental and clinical studies show a need for further investigation of sex-based differences in disease pathophysiology, treatment response, and a sex-specific approach in the development of novel therapeutic methods against myocardial IRI. In this literature review, we summarize the current knowledge on sex differences in the underlying pathophysiological mechanisms of myocardial IRI, including the roles of sex hormones and sex chromosomes. Furthermore, we address sex differences in pharmacokinetics, pharmacodynamics, and pharmacogenetics of current drugs prescribed to limit myocardial IRI. Lastly, we highlight ongoing clinical trials assessing novel pharmacological treatments against myocardial IRI and sex differences that may underlie the efficacy of these new therapeutic approaches.

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The Roles of Testosterone in Cardiac Ischemia/Reperfusion Injury

Apaijai

Chattipakorn

2020

Sex Differences in Heart Disease

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Paradoxical effect of testosterone supplementation therapy on cardiac ischemia/reperfusion injury in aged rats

Cited by 8 publications

References 51 publications

Protective Effect and Mechanism of Dexmedetomidine on Myocardial Ischemia-Reperfusion Injury by Regulating Titin/Myosin Heavy Chain Signal Axis

Protective Effect and Mechanism of Dexmedetomidine on Myocardial Ischemia-Reperfusion Injury by Regulating Titin/Myosin Heavy Chain Signal Axis

Sex Differences in Therapies against Myocardial Ischemia-Reperfusion Injury: From Basic Science to Clinical Perspectives

The Roles of Testosterone in Cardiac Ischemia/Reperfusion Injury

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