The regulatory effect of bromocriptine on cardiac hypertrophy by prolactin and D2 receptor modulation

Aguayo-Cerón, Karla Aidee; Calzada‐Mendoza, Claudia C.; Méndez-Bolaina, Enrique; Romero‐Nava, Rodrigo; Ocharan-Hernández, María Esther

doi:10.1080/10641963.2020.1772814

Cited by 5 publications

(5 citation statements)

References 48 publications

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“…Currently, there are no medications that specifically prevent the development of cardiac hypertrophy, but there are medications to manage the underlying pathology, like systemic arterial hypertension, some of which have been shown to reduce cardiac remodeling typical of the natural history of the disease, among which are angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers [52], and angiotensin receptor-neprilysin inhibitors, and in patients with established heart failure, the use of diuretics like sodium-glucose transporter 2 inhibitors is helpful to reduce symptomatology [54]. The present study evaluated the effect of Zoapatle on the expression of TNF-α, IL-1β, NF-κB, STAT5, and the PRLR in the left ventricle, brain, and renal cortex of rats with ISO-induced ventricular hypertrophy [55]. Our results showed that ISO-induced ventricular hypertrophy increased the gene expression of TNF-α, IL-1β, STAT5, and the PRLR in the left ventricle, while the gene expression of NF-κB was decreased compared with that in the control group.…”

Section: Discussionmentioning

confidence: 96%

Effect of Zoapatle (Montanoa tomentosa) on Inflammatory Markers in a Murine Model of Ventricular Hypertrophy

López-Luna,

Vargas-De-León,

Gutiérrez-Rojas

et al. 2024

Sci. Pharm.

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Zoapatle, a native plant utilized for centuries in traditional Mexican medicine, is abundantly found in Mesoamerica and northern South America. Pleiotropic effects of this genus have been recognized, primarily inducing alterations in smooth muscle contractility in animal models. The aim of this study was to evaluate the effect of Zoapatle on the hypertrophy index and the gene expression of TNF-α, IL-1β, NF-κB, STAT5, and the PRLR in the brain, left ventricle, and renal cortex of rats with isoproterenol-induced cardiac hypertrophy. Three groups were studied, the control group (n = 4), hypertrophy group (n = 4) and hypertrophy group treated with Zoapatle (n = 4). A ventricular hypertrophy model was developed with 150 mg/kg/day of isoproterenol intraperitoneally administered over two days with a 24 h interval between applications. Zoapatle was administered for 28 consecutive days (25 mg/kg). Gene expression was determined with RT-qPCR. Subsequently, a principal component analysis (PCA) was performed using the RNA expression variables. A notably reduced left ventricle mass index was observed in the Zoapatle group. Additionally, Zoapatle administration in cardiac hypertrophy demonstrated a significant decrease in the gene expression of TNF-α, IL-1B, STAT 5, and the PRLR. TNF-α and the transcription factor STAT5 exhibited a similar trend in both the left ventricle and renal cortex, suggesting a correlation with the inflammatory state in these tissues due to ventricular hypertrophy. The findings suggest that Zoapatle reverses the hypertrophy index in a hypertrophy model, concurrently reducing several proinflammatory mediators associated with the hypertrophy index.

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Section: Discussionmentioning

confidence: 96%

Effect of Zoapatle (Montanoa tomentosa) on Inflammatory Markers in a Murine Model of Ventricular Hypertrophy

López-Luna,

Vargas-De-León,

Gutiérrez-Rojas

et al. 2024

Sci. Pharm.

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“…In addition, hyperprolactine-mia is associated with endothelial dysfunction and impaired insulin sensitivity [43,44], increased arterial stiffness [45], and the risk of atherosclerosis and cardiovascular events in high-risk patients [44]. In addition, prolactin receptor expression appears to be linked to myocardial hypertrophy [46]. Although prolactin did not reliably reflect cardiometabolic risk in an analysis of 3232 subjects from the Framingham Heart Study [47], a recent study of 10,907 patients with type 2 diabetes showed a positive association of serum prolactin with mortality [48], and a recent meta-analysis of 14 studies involving 23,596 patients confirmed that serum prolactin is an independent predictor of all-cause mortality and cardiovascular mortality [49].…”

Section: Discussionmentioning

confidence: 99%

Sacubitril/Valsartan Alleviates Cardiac Remodeling and Dysfunction in L-NAME-Induced Hypertension and Hypertensive Heart Disease

Stanko,

Repova,

Baka

et al. 2024

Biomedicines

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There is ample evidence on the benefit of angiotensin receptor-neprilysin inhibitors (ARNIs) in heart failure, yet data regarding the potential protective action of ARNIs in hypertensive heart disease are sparse. The aim of this study was to show whether an ARNI exerts a protective effect in a model of Nω-nitro-L-arginine methyl ester (L-NAME)-induced hypertension with a hypertensive heart and to compare this potential benefit with an angiotensin-converting enzyme inhibitor, captopril. Five groups of adult male Wistar rats were studied (14 per group) for four weeks: untreated controls; ARNI (68 mg/kg/day); L-NAME (40 mg/kg/day); L-NAME treated with ARNI; and L-NAME treated with captopril (100 mg/kg/day). L-NAME administration induced hypertension, accompanied by increased left ventricular (LV) weight and fibrotic rebuilding of the LV in terms of increased concentration and content of hydroxyproline in insoluble collagen and in total collagen and with a histological finding of fibrosis. These alterations were associated with a compromised systolic and diastolic LV function. Treatment with either an ARNI or captopril reduced systolic blood pressure (SBP), alleviated LV hypertrophy and fibrosis, and prevented the development of both systolic and diastolic LV dysfunction. Moreover, the serum levels of prolactin and prolactin receptor were reduced significantly by ARNI and slightly by captopril. In conclusion, in L-NAME-induced hypertension, the dual inhibition of neprilysin and AT1 receptors by ARNI reduced SBP and prevented the development of LV hypertrophy, fibrosis, and systolic and diastolic dysfunction. These data suggest that ARNI could provide protection against LV structural remodeling and functional disorders in hypertensive heart disease.

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“…The silencing of PRLR gene leaded to the inhibition of hippocampal neuron apoptosis, which indicated the role of PRLR in cell apoptosis [ 31 ]. And PRLR protein expression was increased in hypertrophy hearts, and involved in the development of cardiac hypertrophy [ 32 ]. PRLR was also a gene (PRLRa) which played an important role for the regulation of osmotic and related to the abnormal renal development [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

Prenatal diagnosis and mRNA profiles of fetal tetralogy of Fallot

Gou

Zhou²,

Jia³

et al. 2022

BMC Pregnancy Childbirth

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Tetralogy of fallot (TOF) in the fetus is a typical congential heart disease that occurs during the early embryonic period, being characterized by the abnormal development of conus arteriosus. The early diagnosis and prevention of fetal TOF is very important and there is a great need for exploring the pathogenesis of it in clinic. In this study, there were three cases being detected with TOF by fetal echocardiogram and confirmed by autopsy. We characterize the difference of expression of lncRNAs and mRNAs through sequencing analysis of 3 pairs of myocardial tissues of fetal TOF and those of age-matched controls. Compared with normal group, there were 94 differentially expressed lncRNAs and 83 mRNA transcripts in TOF (P < 0.05). Correlation analysis between lncRNA and mRNA further showed that differentially expressed lncRNA can be linked to mRNAs, suggesting the potential regulator role of lncRNA in mRNA expression. Our data serve as a fundamental resource for understanding the disease etiology of TOF.

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The regulatory effect of bromocriptine on cardiac hypertrophy by prolactin and D2 receptor modulation

Cited by 5 publications

References 48 publications

Effect of Zoapatle (Montanoa tomentosa) on Inflammatory Markers in a Murine Model of Ventricular Hypertrophy

Effect of Zoapatle (Montanoa tomentosa) on Inflammatory Markers in a Murine Model of Ventricular Hypertrophy

Sacubitril/Valsartan Alleviates Cardiac Remodeling and Dysfunction in L-NAME-Induced Hypertension and Hypertensive Heart Disease

Prenatal diagnosis and mRNA profiles of fetal tetralogy of Fallot

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