[Cardiometabolic efficacy and toxicological evaluation of a pharmacological galanin receptor agonist]

Biomed Khim. 2019 Apr;65(3):231-238. doi: 10.18097/PBMC20196503231.
[Article in Russian]

Abstract

The goal of this study was to examine effects of a novel galanin receptor agonist GalR1-3 [bAla14, His15]-galanine 2-15 (G), obtained by automatic solid-phase synthesis, on the metabolic state of the area at risk and the size of acute myocardial infarction (MI) in rats in vivo and evaluate its toxicity in BALB /c mice. In anesthetized rats, regional ischemia was simulated by coronary artery occlusion and then coronary blood flow was restored. The peptide G was administered intravenously (i.v.) with a bolus after a period of regional ischemia in the dose range of 0.25-3.0 mg/kg. The sizes of MI and the activities of creatine kinase-MB (СK-MB) and lactate dehydrogenase (LDH) in blood plasma were estimated. The effect of administration of the optimal dose of G (1.0 mg/kg) on myocardial content of adenine nucleotides (AN), phosphocreatine (PCr), creatine (Cr) and lactate was studied. I.v. administration of G to rats at a dose of 1.0 mg/kg slightly affected hemodynamic parameters, but reduced MI size by 40% and decreased plasma LDH and CK-MB activity by the end of reperfusion compared to control. These effects were accompanied by a significant improvement in energy state of area at risk (AAR) - an increase in myocardial content of ATP, åAN, PCr and åCr, and combined with a decrease in myocardial lactate level compared with the control. Toxicity of peptide G was studied with a single intraperitoneal injection of 0.5-3.0% solution of the peptide substance to mice. The absence of signs of intoxication and death of animals after G injection in the maximum possible dose did not allow determining the value of the average lethal dose. The results indicate therapeutic potential of the peptide G for preventing myocardial ischemia and reperfusion injury and feasibility for further study of its pharmacological properties and mechanisms of action.

Tsel' issledovaniia sostoiala v izuchenii vliianiia novogo sinteticheskogo agonista retseptorov galanina GalR1-3 [bAla14, His15]-galanin 2-15 (G), poluchennogo metodom avtomaticheskogo tverdofaznogo sinteza, na metabolicheskoe sostoianie zony riska (ZR) i razmery ostrogo infarkta miokarda (OIM) u krys in vivo i izuchenii ego toksichnosti pri odnokratnom vvedenii mysham linii BALB/s. OIM modelirovali u narkotizirovannykh krys Wistar okkliuzieĭ koronarnoĭ arterii i posleduiushchim vosstanovleniem koronarnogo krovotoka. Peptid G vvodili vnutrivenno (v/v) posle perioda regional'noĭ ishemii v diapazone doz 0,25-3,0 mg/kg. Otsenivali razmery OIM, aktivnost' MV-fraktsii kreatinkinazy (MV-KK) i laktatdegidrogenazy (LDG) v plazme krovi. Izucheno vliianie vvedeniia optimal'noĭ dozy G 1,0 mg/kg na soderzhanie v miokarde adeninnukleotidov (AN), fosfokreatina (FKr), kreatina (Kr) i laktata. Toksichnost' G izuchali pri odnokratnom vnutribriushinnom vvedenii mysham 0,5-3,0% rastvora substantsii peptida. V/v vvedenie G krysam v doze 1,0 mg/kg neznachitel'no izmenialo gemodinamicheskie pokazateli, no umen'shalo razmery OIM na 40% i snizhalo aktivnost' LDG i MV-KK v plazme k kontsu reperfuzii po sravneniiu s kontrolem. Éto soprovozhdalos' dostovernym uluchsheniem metabolicheskogo sostoianiia ZR – uvelicheniem soderzhaniia ATP, obshchego fonda adeninnukleotidov (åAH), FKr, obshchego kreatina (åKr) i snizheniem urovnia laktata. Otsutstvie priznakov intoksikatsii i gibeli zhivotnykh pri odnokratnom vvedenii G v maksimal'no vozmozhnoĭ doze ne pozvolili ustanovit' velichinu dozy LD50. Rezul'taty ukazyvaiut na vozmozhnost' ispol'zovaniia peptida G dlia snizheniia ishemicheskikh i reperfuzionnykh povrezhdeniĭ serdtsa i neobkhodimost' dal'neĭshego izucheniia ego farmakologicheskikh svoĭstv i mekhanizmov deĭstviia.

Keywords: modified galanin fragment; myocardial energy metabolism; myocardial ischemia and reperfusion; rat; toxicity.

MeSH terms

  • Animals
  • Creatine Kinase, MB Form / blood
  • Disease Models, Animal
  • L-Lactate Dehydrogenase / blood
  • Mice
  • Mice, Inbred BALB C
  • Myocardial Infarction / drug therapy
  • Myocardial Infarction / pathology*
  • Myocardial Reperfusion Injury / drug therapy
  • Myocardial Reperfusion Injury / pathology
  • Peptides / pharmacology*
  • Rats
  • Receptors, Galanin / agonists*

Substances

  • Peptides
  • Receptors, Galanin
  • L-Lactate Dehydrogenase
  • Creatine Kinase, MB Form