Cardioprotective Effect of Flibanserin against Isoproterenol-Induced Myocardial Infarction in Female Rats: Role of Cardiac 5-HT2A Receptor Gene/5-HT/Ca2+ Pathway

Ahmed, Mohamed I.; Abdelrazek, Heba M. A.; Moustafa, Yasser M.; Alshawwa, Samar Zuhair; Mobasher, Maysa A.; Abdel-Wahab, Basel A.; Abdelgawad, Fathy Elsayed; Khodeer, Dina M.

doi:10.3390/ph16040502

Cited by 6 publications

(3 citation statements)

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“…It is already approved for the treatment of hypoactive sexual desire disorder. Treatment with flibanserin evoked strong cardioprotective effects in a dose-dependent manner in an isoproterenol-induced model of AMI in rats . In this study, flibanserin treatment lowered heart rate, preserved architecture of myocardial fibers, and reduced 5-HT2AR expression in the cardiac tissue.…”

Section: -Ht2rsupporting

confidence: 52%

“…Treatment with flibanserin evoked strong cardioprotective effects in a dose-dependent manner in an isoproterenol-induced model of AMI in rats. 69 In this study, flibanserin treatment lowered heart rate, preserved architecture of myocardial fibers, and reduced 5-HT2AR expression in the cardiac tissue. However, flibanserin was given orally (45 mg/ kg) for 4 weeks prior to AMI-induction, rather as a protective measure than post-AMI treatment, and the end-point of this study was only 1 day post AMI-induction.…”

Section: ■ 5-ht2rmentioning

confidence: 50%

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Serotonin Receptors in Myocardial Infarction: Friend or Foe?

Bahr,

Ricke-Hoch,

Ponimaskin

et al. 2024

ACS Chem. Neurosci.

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Acute myocardial infarction (AMI) is one of the leading causes of death worldwide and treatment costs pose a major burden on the global health care system. Despite the variety of treatment options, individual recovery can be still poor and the mortality rate, especially in the first few years after the event, remains high. Therefore, intense research is currently focused on identifying novel target molecules to improve the outcome following AMI. One of the potentially interesting targets is the serotonergic system (5-HT system), not at least because of its connection to mental disorders. It is known that patients suffering from AMI have an increased risk of developing depression and vice versa. This implicates that the 5-HT system can be affected in response to AMI and might thus represent a target structure for patients' treatment. This review aims to highlight the importance of the 5-HT system after AMI by describing the role of individual serotonin receptors (5-HTR) in the regulation of physiological and pathophysiological responses. It particularly focuses on the signaling pathways of the serotonin receptors 1, 2, 4, and 7, which are expressed in the cardiovascular system, during disease onset, and the following remodeling process. This overview also emphasizes the importance of the 5-HT system in AMI etiology and highlights 5-HTRs as potential treatment targets.

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Section: -Ht2rsupporting

confidence: 52%

Section: ■ 5-ht2rmentioning

confidence: 50%

Serotonin Receptors in Myocardial Infarction: Friend or Foe?

Bahr,

Ricke-Hoch,

Ponimaskin

et al. 2024

ACS Chem. Neurosci.

View full text Add to dashboard Cite

show abstract

“…Heavy metals such as lead, mercury, cadmium, and arsenic, ubiquitous in the environment due to industrial and technological activities, pose a significant health risk. 5 , 6 The exact mechanisms through which heavy metals contribute to CVD are not fully understood, but prevailing theories suggest that impaired antioxidant metabolism and oxidative stress might be key pathways. Oxidative stress, resulting from an imbalance between the production of reactive oxygen species and the body’s ability to detoxify these harmful intermediates, is a recognized contributor to the pathogenesis of CVD.…”

Section: Introductionmentioning

confidence: 99%

Cardioprotective Effects of α-Asarone Against Hexavalent Chromium-Induced Oxidative Damage in Mice

Alwaili,

Elhoby,

El-Sayed

et al. 2024

DDDT

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Introduction This comprehensive study investigated the therapeutic potential of α-asarone in mitigating myocardial oxidative damage, primarily induced by hexavalent chromium (Cr(VI)) exposure in mice. Methods In this experiment, 24 mice were divided into four groups to assess the cardioprotective role of α-asarone. The study focused on two treatment groups, receiving 25 mg and 50 mg of α-asarone, respectively. These groups were compared against a control group subjected to Cr(VI) without α-asarone treatment, and a normal control negative group. The key biochemical parameters evaluated included serum levels of Creatine Kinase-MB (CK-MB) and Troponin I, markers indicative of myocardial damage. Additionally, the levels of Malondialdehyde (MDA) were measured to assess lipid peroxidation, alongside the evaluation of key inflammatory biomarkers in cardiac tissue homogenates, such as Tumor Necrosis Factor-α (TNF-α) and Interleukin-1β (IL-1β). Results Remarkably, α-asarone treatment resulted in a significant reduction in these markers compared to the control group. The treatment also elevated the activity of cardinal antioxidant enzymes like catalase (CAT) and superoxide dismutase (SOD), and reduced the glutathione (GSH). Furthermore, a notable upregulation of Peroxisome Proliferator-Activated Receptor Gamma (PPAR-γ) in cardiac tissue homogenates was observed, highlighting a potential pathway through which α-asarone exerts its protective effects. Histopathological analysis of cardiac tissues revealed that α-asarone ameliorated the structural lesions induced by Cr(VI). The study thus provides substantial evidence that α-asarone ameliorates Cr(VI)-induced cardiotoxicity through a multifaceted approach. It enhances cardiac enzyme function, modulates free radical generation, improves antioxidant status, and mitigates histopathological damage in cardiac tissues. Given these findings, α-asarone emerges as a promising agent against Cr(VI)-induced myocardial injury. Purpose This study paves the way for further research into the cardioprotective properties of α-asarone and its potential application in clinical settings by specifically exploring the protective efficacy of α-asarone against Cr(VI)-induced cardiotoxicity and delineating the underlying biochemical and molecular mechanisms involved.

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