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Drug Res (Stuttg) 2023; 73(02): 105-112
DOI: 10.1055/a-1967-2004
Original Article

Effect Produced by a Cyclooctyne Derivative on Both Infarct Area and Left Ventricular Pressure via Calcium Channel Activation

Figueroa-Valverde Lauro
1   Laboratory of Pharmaco-Chemistry, Faculty of Chemical Biological Sciences, University Autonomous of Campeche, Av. Agustín Melgar s/n, Col Buenavista C.P. Campeche, Camp., México.
,
Rosas-Nexticapa Marcela
2   Facultad de Nutrición, Universidad Veracruzana, Médicos y Odontologos s/n C.P. Unidad del Bosque Xalapa Veracruz, México.
,
López-Ramos Maria
1   Laboratory of Pharmaco-Chemistry, Faculty of Chemical Biological Sciences, University Autonomous of Campeche, Av. Agustín Melgar s/n, Col Buenavista C.P. Campeche, Camp., México.
,
Díaz-Cedillo Francisco
3   Escuela Nacional de Ciencias Biológicas del Instituto Politécnico Nacional. Prol. Carpio y Plan de Ayala s/n Col. Santo Tomas, México, D.F. C.P.
,
Alvarez-Ramirez Magdalena
3   Escuela Nacional de Ciencias Biológicas del Instituto Politécnico Nacional. Prol. Carpio y Plan de Ayala s/n Col. Santo Tomas, México, D.F. C.P.
,
Mateu-Armad Maria Virginia
3   Escuela Nacional de Ciencias Biológicas del Instituto Politécnico Nacional. Prol. Carpio y Plan de Ayala s/n Col. Santo Tomas, México, D.F. C.P.
,
Melgarejo-Gutierrez Montserrat
4   Facultad de Medicine, Universidad Veracruzana, Médicos y Odontologos s/n C.P. Unidad del Bosque Xalapa Veracruz, México
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Abstract

Background There are reports which indicate that some cyclooctyne derivatives may exert changes in cardiovascular system; however, its molecular mechanism is not very clear.

Objective The aim of this study was to evaluate the biological activity of four cyclooctyne derivatives (compounds 1 to 4) produced on infarct area and left ventricular pressure.

Methods Biological activity produced by cyclooctyne derivatives on infarct area was determinate using an ischemia/reperfusion injury model. In addition, to characterize the molecular mechanism of this effect, the following strategies were carried out as follows; i) biological activity produced by cyclooctyne derivative (compound 4) on either perfusion pressure or left ventricular pressure was evaluated using an isolated rat heart; ii) theoretical interaction of cyclooctyne derivative with calcium channel (1t0j protein surface) using a docking model.

Results The results showed that cyclooctyne derivative (compound 4) decrease infarct area of in a dose-dependent manner compared with compound 1 to 3. Besides, this cyclooctyne derivative increase both perfusion pressure and left ventricular pressure which was inhibited by nifedipine. Other theoretical data suggests that cyclooctyne derivative could interact with some aminoacid residues (Met83, Ile85, Ser86, Leu108, Glu114) involved in 1t0j protein surface.

Conclusions All these data indicate that cyclooctyne derivative increase left ventricular pressure via calcium channel activation and this phenomenon could be translated as a decrease of infarct area.

Key words

Cyclooctyne - derivative - infarct - ischemia - calcium channel.


Publication History

Received: 11 September 2022

Accepted: 10 October 2022

Article published online:
29 November 2022

© 2022. Thieme. All rights reserved.

Georg Thieme Verlag
Rüdigerstraße 14, 70469 Stuttgart, Germany

 

  • References

  • 1 Sarajlic P, Simonsson M, Jernberg T. et al. Incidence, associated outcomes, and predictors of upper gastrointestinal bleeding following acute myocardial infarction: a SWEDEHEART-based nationwide cohort study. Eur Heart J Cardiov Pharmacother 2022; 8: 483-491
    CrossrefPubMedGoogle Scholar
  • 2 Sagris M, Antonopoulos A, Theofilis P. et al. Risk factors profile of young and older patients with Myocardial Infarction. Cardiovasr Res 2022; 118: 2281-2292
    CrossrefPubMedGoogle Scholar
  • 3 Moledina S, Shoaib A, Weston C. et al. Ethnic disparities in care and outcomes of non-ST-segment elevation myocardial infarction: a nationwide cohort study. Eur Heart J-Q Care Clin Out 2022; 8: 518-528
    PubMedGoogle Scholar
  • 4 Collard C, Gelman S. Pathophysiology, clinical manifestations, and prevention of ischemia-reperfusion injury. J Ame Soc Anesth 2001; 94: 1133-1138
    PubMedGoogle Scholar
  • 5 Yellon D, Hausenloy D. Myocardial reperfusion injury. New Engl J Med 2007; 357: 1121-1135
    CrossrefPubMedGoogle Scholar
  • 6 Van’t Hof A, Liem A, Suryapranata H. et al. Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction: myocardial blush grade. Circulation 1998; 97: 2302-2306
    CrossrefPubMedGoogle Scholar
  • 7 Verma S, Fedak P, Weisel R. et al. Fundamentals of reperfusion injury for the clinical cardiologist. Circulation 2002; 105: 2332-2336
    CrossrefPubMedGoogle Scholar
  • 8 Liu H, Wang C, Qiao Z. et al. Protective effect of curcumin against myocardium injury in ischemia reperfusion rats. Pharm Biol 2017; 55: 1144-1148
    CrossrefPubMedGoogle Scholar
  • 9 Yaoita H, Ogawa K, Maehara K. et al. Attenuation of ischemia/reperfusion injury in rats by a caspase inhibitor. Circulation 1998; 97: 276-281
    CrossrefPubMedGoogle Scholar
  • 10 Liang Z, Liu L, Yao T. et al. Cardioprotective effects of Guanxinshutong (GXST) against myocardial ischemia/reperfusion injury in rats. J Geriat Cardiol 2012; 9: 130
    CrossrefPubMedGoogle Scholar
  • 11 Fancelli D, Abate A, Amici R. et al. Cinnamic anilides as new mitochondrial permeability transition pore inhibitors endowed with ischemia-reperfusion injury protective effect in vivo. J Med Chem 2014; 57: 5333-5347
    CrossrefPubMedGoogle Scholar
  • 12 Van Zandt M, Whitehouse D, Golebiowski A. et al. Discovery of (R)-2-amino-6-borono-2-(2-(piperidin-1-yl) ethyl) hexanoic acid and congeners as highly potent inhibitors of human arginases I and II for treatment of myocardial reperfusion injury. J Med Chem 2013; 56: 2568-2580
    CrossrefPubMedGoogle Scholar
  • 13 Zhang H, Zhang R, Liao X. et al. Discovery of β-Carboline Derivatives as a Highly Potent Cardioprotectant against Myocardial Ischemia-Reperfusion Injury. J Med Chem 2021; 64: 9166-9181
    CrossrefPubMedGoogle Scholar
  • 14 Clark J, Gebhart G, Gonder J. et al. The 1996 guide for the care and use of laboratory animals. ILAR J 1997; 38: 41-48
    CrossrefPubMedGoogle Scholar
  • 15 Figueroa-Valverde L, Diaz-Cedillo F, Rosas-Nexticapa M. et al. Synthesis and biological activity of two oxireno-azecin-imidazole derivatives on perfusion pressure via guanylate cyclase inhibition. Biointer Resin Appl Chem 2018; 3543-3551
    PubMedGoogle Scholar
  • 16 Figueroa-Valverde L, Diaz-Cedillo F, Rosas-Nexticapa M. et al. Synthesis and Biological Activity of a Bis-steroid-methanocyclobuta-naphthalene-dione Derivative against Ischemia/Reperfusion Injury via Calcium Channel Activation. Anti-Inflam Anti-Allergy Agents Med Chem 2020; 19: 393-412
    CrossrefPubMedGoogle Scholar
  • 17 Quirk T. One-way analysis of variance (ANOVA). InExcel 2007 for educational and psychological statistics. 2012. Springer; New York, NY:
    Google Scholar
  • 18 Sherikar A, Bhatia M, Dhavale R. Identification and Investigation of Chalcone Derivatives as Calcium Channel Blockers: Pharmacophore Modeling, Docking Studies, In vitro Screening, and 3D-QSAR Analysis. Curr Comp-Aid Drug Des 2021; 17: 676-686
    CrossrefPubMedGoogle Scholar
  • 19 Torchala M, Gerguri T, Chaleil R. et al. Enhanced sampling of protein conformational states for dynamic cross-docking within the protein-protein docking server SwarmDock. Proteins:Struct Funct Bioinform 2020; 88: 962-972
    PubMedGoogle Scholar
  • 20 Markwardt F, Nilius B. Modulation of calcium channel currents in guinea-pig single ventricular heart cells by the dihydropyridine Bay K 8644. J Physiol 1988; 399: 559-575
    CrossrefPubMedGoogle Scholar
  • 21 Yamaguchi M, Murata T, Ramos J. The calcium channel agonist Bay K 8644 promotes the growth of human liver cancer HepG2 cells in vitro: suppression with overexpressed regucalcin. Mol Cell Biochem 2020; 472: 173-185
    CrossrefPubMedGoogle Scholar
  • 22 Figueroa-Valverde L, Rosas-Nexticapa M, Montserrat M. et al. Synthesis and Theoretical Interaction of 3-(2-oxabicyclo [7.4. 0] trideca-1 (13), 9, 11-trien-7-yn-12-yloxy)-steroid Deriva-tive with 17β-hydroxysteroid Dehydrogenase Enzyme Surface. Biointerface Res Appl Chem 2023; 13: 266
    PubMedGoogle Scholar
  • 23 Figueroa-Valverde L, Diaz-Cedillo F, Gobato R. et al. Design and synthesis of two Strychnidin-oxiran-naphthalenol derivatives and their theoretical evaluation as noradrenaline and serotonin reuptake inhibitors. Vietnam Journal of Chemistry 2022; 60: 245-256
    PubMedGoogle Scholar
  • 24 Lagunin A, Gloriozova T, Dmitriev A. et al. Computer evaluation of drug interactions with P-glycoprotein. Bull Exp Biol Med 2013; 154: 521-524
    CrossrefPubMedGoogle Scholar
  • 25 Banerjee P, Eckert A, Schrey A. et al. ProTox-II: a webserver for the prediction of toxicity of chemicals. Nucleic Acids Res 2018; 46: W257-W263
    CrossrefPubMedGoogle Scholar
  • 26 Bi W, Bi Y, Xue P. et al. Novel β-carboline-tripeptide conjugates attenuate mesenteric ischemia/reperfusion injury in the rat. Eur J Med Chem 2011; 46: 2441-2452
    CrossrefPubMedGoogle Scholar
  • 27 Zocchi C, Ongini E, Conti A. et al. The non-xanthine heterocyclic compound SCH 58261 is a new potent and selective A2a adenosine receptor antagonist. J Pharmacol Exp Ther 1996; 276: 398-404
    PubMedGoogle Scholar
  • 28 Sato Y, Shimoji Y, Fujita H. et al. Studies on cardiovascular agents. 6. Synthesis and coronary vasodilating and antihypertensive activities of 1, 2, 4-triazolo [1, 5-a] pyrimidines fused to heterocyclic systems. J Med Chem 1980; 23: 927-937
    CrossrefPubMedGoogle Scholar
  • 29 Stavrovskaya I, Narayanan M, Zhang W. et al. Clinically approved heterocyclics act on a mitochondrial target and reduce stroke-induced pathology. J Exp Med 2004; 200: 211-222
    CrossrefPubMedGoogle Scholar
  • 30 Mitsuyama T, Kawamata T, Yamane F. et al. Role of a synthetic pyrimidine compound, MS-818, in reduction of infarct size and amelioration of sensorimotor dysfunction following permanent focal cerebral ischemia in rats. J Neuros 2002; 96: 1072-1076
    CrossrefPubMedGoogle Scholar
  • 31 Mohsin Alvi A, Tariq Al Kury L, Umar Ijaz M. et al. Post-treatment of synthetic polyphenolic 1, 3, 4 oxadiazole compound A3, attenuated ischemic stroke-induced neuroinflammation and neurodegeneration. Biomol 2020; 10: 816
    PubMedGoogle Scholar
  • 32 Salloum F, Ockaili R, Wittkamp M. et al. Vardenafil: a novel type 5 phosphodiesterase inhibitor reduces myocardial infarct size following ischemia/reperfusion injury via opening of mitochondrial KATP channels in rabbits. J Mol Cell Cardiol 2006; 40: 405-411
    CrossrefPubMedGoogle Scholar
  • 33 Imai S, Katano Y, Nakazawa M. et al. The effects of norepinephrine on the release of cyclic AMP by the isolated perfused heart of the guinea pig. Life Sci 1978; 23: 1609-1617
    CrossrefPubMedGoogle Scholar
  • 34 Salden F, Luermans J, Westra S. et al. Short-term hemodynamic and electrophysiological effects of cardiac resynchronization by left ventricular septal pacing. J Am Coll Cardiol 2020; 75: 347-359
    CrossrefPubMedGoogle Scholar
  • 35 Weishaar R, Kobylarz-Singer D, Steffen R. et al. Subclasses of cyclic AMP-specific phosphodiesterase in left ventricular muscle and their involvement in regulating myocardial contractility. Circulation Res 1987; 61: 539-547
    CrossrefPubMedGoogle Scholar
  • 36 Kisch-Wedel H, Kemming G, Meisner F. et al. The prostaglandins epoprostenol and iloprost increase left ventricular contractility in vivo. Intens Care Med 2003; 29: 1574-1583
    CrossrefPubMedGoogle Scholar
  • 37 Kisch-Wedel H, Kemming G, Meisner F. et al. Effect of prostaglandin I2 analogues on left ventricular diastolic function in vivo. Eur J Pharmacol 2005; 517: 208-216
    CrossrefPubMedGoogle Scholar
  • 38 Higgins C, Vatner S, Franklin DEAN, Braunwald EUGENE. Effects of prostaglandin A 1 on left ventricular dynamics in the conscious dog. Am J Physiol-Leg Cont 1972; 222: 1534-1538
    CrossrefPubMedGoogle Scholar
  • 39 Degousee N, Fazel S, Angoulvant D. et al. Microsomal prostaglandin E2 synthase-1 deletion leads to adverse left ventricular remodeling after myocardial infarction. Circulation 2008; 117: 1701-1710
    CrossrefPubMedGoogle Scholar
  • 40 Meena V, Meena D, Rathore P. et al. Comparison of the efficacy and safety of indomethacin, ibuprofen, and paracetamol in the closure of patent ductus arteriosus in preterm neonates-A randomized controlled trial. Ann Pediat Cardiol 2020; 13: 130
    CrossrefPubMedGoogle Scholar
  • 41 Tan S, Shapiro R, Franco R. et al. Indomethacin-induced prostaglandin inhibition with hyperkalemia: a reversible cause of hyporeninemic hypoaldosteronism. Ann Int Med 1979; 90: 783-785
    CrossrefPubMedGoogle Scholar
  • 42 Von der Saal W, Hoelck J, Kampe W. et al. Nonsteroidal cardiotonics. 2. The inotropic activity of linear, tricyclic 5-6-5 fused heterocycles. J Med Chem 1989; 32: 1481-1491
    CrossrefPubMedGoogle Scholar
  • 43 Figueroa-Valverde L, Lopez-Ramos M, Rosas-Nexticapa M. et al. Experimental, theoretical and biological activity of a triazonine-derivative on left ventricular pressure. Cardiovasc Hematol Agents Med Chemy 2016; 14: 125-133
    CrossrefPubMedGoogle Scholar
  • 44 Lorell B, Paulus W, Grossman W. et al. Modification of abnormal left ventricular diastolic properties by nifedipine in patients with hypertrophic cardiomyopathy. Circulation 1982; 65: 499-507
    CrossrefPubMedGoogle Scholar
  • 45 Joshi P, Dalal J, Ruttley M. et al. Nifedipine and left ventricular function in beta-blocked patients. Heart 1981; 45: 457-459
    CrossrefPubMedGoogle Scholar
  • 46 Paulus W, Lorell B, Craig W. et al. Comparison of the effects of nitroprusside and nifedipine on diastolic properties in patients with hypertrophic cardiomyopathy: altered left ventricular loading or improved muscle inactivation?. J Am Coll Cardiol 1983; 2: 879-886
    CrossrefPubMedGoogle Scholar
  • 47 Liu Y, Grimm M, Dai W. et al. CB-Dock: a web server for cavity detection-guided protein-ligand blind docking. Acta Pharmacol Sinica 2020; 41: 138-144
    CrossrefPubMedGoogle Scholar
  • 48 Kasmi R, Hadaji E, Chedadi O. et al. 2D-QSAR and docking study of a series of coumarin derivatives as inhibitors of CDK (anticancer activity) with an application of the molecular docking method. Heliyon 2020; 6: e04514
    CrossrefPubMedGoogle Scholar
  • 49 Zhang W, Bell E, Yin M. et al. EDock: blind protein–ligand docking by replica-exchange monte carlo simulation. J Cheminform 2020; 12: 1-17
    CrossrefPubMedGoogle Scholar
  • 50 Torchala M, Gerguri T, Chaleil R. et al. Enhanced sampling of protein conformational states for dynamic cross-docking within the protein-protein docking server SwarmDock. Protein Struct Funct Bioinform 2020; 88: 962-972
    CrossrefPubMedGoogle Scholar
  • 51 Kong R, Yang G, Xue R. et al. COVID-19 Docking Server: A meta server for docking small molecules, peptides and antibodies against potential targets of COVID-19. Bioinform 2020; 36: 5109-5111
    CrossrefPubMedGoogle Scholar
  • 52 Quignot C, Postic G, Bret H. et al. InterEvDock3: a combined template-based and free docking server with increased performance through explicit modeling of complex homologs and integration of covariation-based contact maps. Nucleic Acids Res 2021; 49: W277-W284
    CrossrefPubMedGoogle Scholar
  • 53 Xu X, Zou X. Predicting Protein-Peptide Complex Structures by Accounting for Peptide Flexibility and the Physicochemical Environment. J Chem Inform Model 2021; 62: 27-39
    CrossrefPubMedGoogle Scholar
  • 54 Hu H, Wang Z, Wei R. et al. The molecular architecture of dihydropyrindine receptor/L-type Ca2+channel complex. Sci Rep 2015; 5: 1-6
    CrossrefPubMedGoogle Scholar
  • 55 Rutwick Surya U, Praveen N. A molecular docking study of SARS-CoV-2 main protease against phytochemicals of Boerhavia diffusa Linn. For novel COVID-19 drug discovery. Virus Dis 2021; 32: 46-54
    CrossrefPubMedGoogle Scholar
  • 56 Kumar A, Srivastava G, Negi A. et al. Docking, molecular dynamics, binding energy-MM-PBSA studies of naphthofuran derivatives to identify potential dual inhibitors against BACE-1 and GSK-3β. J Biomol Struc Dyn 2019; 37: 275-290
    CrossrefPubMedGoogle Scholar
  • 57 Levitt D. PK Quest: a general physiologically based pharmacokinetic model. Introduction and application to propranolol. BMC Clin Pharmacol 2002; 2: 1-21
    CrossrefPubMedGoogle Scholar
  • 58 Ishaku S, Bakare-55 Odunola, M Musa A, et al. Effect of dihydro-artemisinin on the pharmacokinetics of gliclazide in diabetic subjects. Int J Biol Chem Sci 2020; 14: 2267-2276
    PubMed
  • 59 Sicak Y. Design and antiproliferative and antioxidant activities of furan-based thiosemicarbazides and 1, 2, 4-triazoles: their structure-activity relationship and SwissADME predictions. Med Chem Res 2021; 30: 1557-1568
    CrossrefPubMedGoogle Scholar