Actividad inducida por androsterona y hemisuccinato de androsterona sobre la presión de perfusión y la resistencia vascular

Figueroa, Lauro; Díaz, Francisco; Camacho, Abelardo; Díaz, E. Llorente; Marvin, Rolando

doi:10.7705/biomedica.v29i4.140

Cited by 7 publications

(2 citation statements)

References 39 publications

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“…The compounds N 1 -(2,3-dimethoxystrychnidin-10-yliden)ethane-1,2-diamine (1) and androsteron-ehemisuccinate (2) were prepared according to a previously reported method of Figueroa 10,12 . The other compounds evaluated in this study were purchased from Sigma-Aldrich Co. Ltd.…”

Section: Methodsmentioning

confidence: 99%

A Facile Synthesis of Two Brucine-Steroid Derivatives

Figueroa‐Valverde

Cedillo²,

Elodia

et al. 2013

Asian J. Chem.

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There are studies which show that several derivatives of brucine have been developed for its use in different biological and analytical methods 1-4. For example, a report shows the synthesis of N-chloromethylbrucine chloride by the reaction of brucine with dichloromethane 5. Other studies have shown the preparation of a brucine derivative (brucidine) by electrolytic reduction of brucine 6. In addition, there are reports of the synthesis of N-(5-carboxypentyl)brucinium bromide via N-alkylation of brucine with 6-bromohexanoic acid 7. Other experimental data showed the preparation of compounds brucinium hydrogen (S)-malate pentahydrate and anhydrous brucinium hydrogen (2R,3R)-tartrate by the reaction between brucine and D-L-malic acid or L-tartaric acid in ethanol:water 8. Additionally, the porphyrin-brucine conjugates was synthetized by the N-alkylation of brucine with alkylbromotetraphenylporphyrin derivatives 9. Recently, a brucine derivative (N 1-(2,3-dimethoxy strychnidin-10-yliden)-ethane-1,2-diamine) was synthetized by the reaction of brucine and ethylenediamine using boric acid as catalyst. Also other brucine derivative (11-[(2-aminoethylamino)-methyl]-2,3-dimethoxystrychnidin-10-ona) was prepared by the reaction of brucine with ethylenediamine in presence of formaldehyde 10. Additionally, other study showed the synthesis of a brucine-dihydropirymidine derivative using the multi-component system (brucine, benzaldehyde and

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Section: Methodsmentioning

confidence: 99%

A Facile Synthesis of Two Brucine-Steroid Derivatives

Figueroa‐Valverde

Cedillo²,

Elodia

et al. 2013

Asian J. Chem.

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“…The results showed that indomethacin did not block the effects of estradiol-ethylenediamine derivative, suggesting that mechanism was not via prostanglandins synthesis and secretion. Analyzing these data and reports indicating that the effect of a number of steroids on blood pressure involves activation of the calcium channel 37 , we used nifedipine an L-type calcium channel inhibitor. The results showed that the activity of estradiol-ethylenediamine derivative was significantly blocked by nifedipine.…”

Section: Discussionmentioning

confidence: 99%

Changes Induced by Estradiol-Ethylenediamine Derivative on Perfusion Pressure and Coronary Resistance in Isolated Rat Heart: L-Type Calcium Channel

Figueroa‐Valverde¹,

Cedillo²,

Ramos³

et al. 2011

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

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Aim. The present study was designed to investigate the effects of estradiol-ethylenediamine derivative on perfusion pressure and coronary resistance in rats. An additional aim was to identify the molecular mechanisms involved.Methods. The Langendorff model was used to measure perfusion pressure and coronary resistance changes in isolated rat heart after estradiol-ethylenediamine derivative alone and following compounds; tamoxifen (estrogen receptor antagonist), prazosin (alpha1 adrenoreceptor antagonist), metoprolol (selective beta1 receptor blocker), indomethacin (prostanglandin synthesis inhibitor) and nifedipine (L-type calcium-channel inhibitor).Results. The results show that estradiol-ethylenediamine derivative [10 -9 mmol] significantly increased perfusion pressure (p = 0.005) and coronary resistance (p = 0.006) in isolated rat heart. Additionally, the effect of estradiolethylenediamine on perfusion pressure [10 -9 to 10 -4 mmol] was only blocked in the presence of the L-type calciumchannel (nifedipine).Conclusions. These data suggest that the effect of estradiol-ethylenediamine on perfusion pressure and vascular coronary involves activation of the L-type calcium channel through a non-genomic molecular mechanism.

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The Decreased Proliferation Capacity of Cardiomyocytes Induced By Androsterone Is Mediated By the Interactions Between Androgen Receptor and Retinoblastoma Protein

Huo,

Wang,

Bai

et al. 2024

J Biochem & Molecular Tox

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Our previous study has demonstrated that the decline in cardiomyocytes proliferation capacity induced by maternal androgen excess was mainly attributed to the accumulation of androsterone in the heart. However, the underlying mechanism by which androsterone inhibits cardiomyocytes proliferation remains unknown. In this study, pregnant mice were injected subcutaneously daily with dihydrotestosterone (DHT) from gestational day (GD) 16.5 to GD18.5. On GD18.5, fetal heart tissue was dissected and used for analyzing androgen receptor (AR) levels. H9c2 cells and primary cardiomyocytes, isolated from fetal hearts, were applied to investigate the mechanism. H9c2 cells under androsterone treatment were subjected to RNA sequencing analysis and the results showed that genes were primarily enriched in cell cycle and DNA replication pathways. Elevated AR levels were observed in fetal cardiac tissue in the maternal DHT‐treated group. Androsterone treatment increased the ratio of nuclear AR and cytoplasmic AR both in H9c2 cells and primary cardiomyocytes. The ablation and overexpression of AR can mildly reverse and aggravate cell cycle arrest induced by androsterone, respectively. ChIP‐qPCR analysis suggested that AR can directly repress cell cycle and DNA replication‐related gene expression, which was mediated by the recruitment of retinoblastoma protein (Rb). The repression of cell proliferation in response to androsterone was alleviated partly through the downregulation of Rb by siRNA transfection. In conclusion, AR repression to cell cycle and DNA replication‐related gene expression, mediated by recruitment of Rb, may be one of the potential mechanisms of cell cycle arrest in cardiomyocytes induced by androsterone.

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Actividad inducida por androsterona y hemisuccinato de androsterona sobre la presión de perfusión y la resistencia vascular

Cited by 7 publications

References 39 publications

A Facile Synthesis of Two Brucine-Steroid Derivatives

A Facile Synthesis of Two Brucine-Steroid Derivatives

Changes Induced by Estradiol-Ethylenediamine Derivative on Perfusion Pressure and Coronary Resistance in Isolated Rat Heart: L-Type Calcium Channel

The Decreased Proliferation Capacity of Cardiomyocytes Induced By Androsterone Is Mediated By the Interactions Between Androgen Receptor and Retinoblastoma Protein

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