Saturskaya A.S.
Change of tumor necrosis factor-alpha concentration on modelling diffuse cardiosclerosis in rats with different resistance to hypoxia
Ternopil State Medical University named after I.Y. Gorbachev, the Ukraine
Abstract.
The article presents the analysis of the results of an experimental study of the changes of tumor necrosis factor-alpha (TNF-T) concentration in the blood serum in the development of diffuse cardiosclerosis in rats with different resistance to hypoxia. The experiments were conducted on 96 experimental white male rats which were divided into experimental groups with different resistance to exogenous hypobaric hypoxia. The experimental model of diffuse cardiosclerosis (DCS) was simulated. Experimentally it has been proved that, in the development of DCS, TNF-T concentration in the blood serum of animals increases significantly after 7 days of modelling. TNF-T concentration in the blood serum is maintained at a high level throughout the next stages of observation: 14 days and 30 days of DCS. The study has shown that the intensity of TNF-T concentration increase in the blood serum of animals in the groups with different resistance to hypoxia varies: it is the greatest in animals with low resistance to hypoxia and the lowest in animals with high resistance to hypoxia. This pattern is observed at all stages of observation, being most clearly marked in the early period of cardiosclerotic process. The data obtained have been analyzed with the use of the latest scientific achievements in the given field.
Key words: hypoxia, diffuse cardiosclerosis, tumor necrosis factor-alpha.
References
1. Song Z, Bai J, Zhang L, Sun X, Zhang M, Zheng H, Zhang J. Effects of telmisartan on inflammation and fibrosis after acute myocardial infarction in rats. Zhonghua Yi Xue Za Zhi. 2014 Sep 9;94(33):2628-33.
2. Iglezias SD, Benvenuti LA, Calabrese F, Salemi VM, Silva AM, Carturan E, de Oliveira SA, Thiene G, De Brito T. Endomyocardial fibrosis: pathological and molecular findings of surgically resected ventricular endomyocardium. Virchows Arch. 2008 Sep;453(3):233-41.
3. Salemi1 VMC, Leite JJ, Picard MH, Oliveira LM, Reisl SF, Pena1 JLB, Mady C. Echocardiographic predictors of functional capacity in endomyocardial fibrosis patients. Eur J Echocardiogr. 2009;10(3):400–5.
4. Kuusisto J, Kärjä V, Sipola P, Kholová I, Peuhkurinen K, Jääskeläinen P, Naukkarinen A, Ylä-Herttuala S, Punnonen K, Laakso M. Low-grade inflammation and the phenotypic expression of myocardial fibrosis in hypertrophic cardiomyopathy. Heart. 2012 Jul;98(13):1007-13.
5. Westermann D. Does inflammation trigger fibrosis in hypertrophic cardiomyopathy: a burning question? Heart. Heart. 2012 Jul;98(13):965-6.
6. Nian M, Lee P, Khaper N, Liu P. Inflammatory cytokines and postmyocardial infarction remodeling. Circ Res. 2004 Jun;94(12):1543-53.
7. Sennikov SV, Silkov AN. Metody opredeleniia tsitokinov [Methods of definition of cytokines]. Tsitokiny i vospalenie. 2005;4(1):22–7.
8. Saturskaya AS. Osobennosti balansa pro- i protivovospalitel'nykh tsitokinov pri eksperimental'nom diffuznom kardioskleroze u krys v zavisimosti ot ikh vrozhdennoi ustoichivosti k gipoksii [Elektronnyi resurs] [Features of balance about - and antiinflammatory cytokines at an experimental diffuse cardiosclerosis at rats depending on their congenital fastness to a hypoxia]. Matematicheskaia morfologiia. Elektronnyi matematicheskii i mediko-biologicheskii zhurnal. 2015;14(1). Rezhim dostupa: http://www.smolensk.ru/user/sgma/MMORPH/N-45-html/saturskaya/saturskaya.htm
9. Saturskaya AS, Bondarenko YuI, Pelykh VE. Izmeneniia tsitokinovogo profilia krovi pri eksperimental'nom diffuznom kardioskleroze u krys s razlichnoi ustoichivost'iu k gipoksii [Changes of a cytokine profile of a blood at an experimental diffuse cardiosclerosis at rats with various fastness to a hypoxia]. Journal of Education, Health and Sport. 2015;5(2):66–78.
10. Wang XJ, Feng CW, Li M. ADAM17 mediates hypoxia-induced drug resistance in hepatocellular carcinoma cells through activation of EGFR/PI3K/Akt pathway. Mol Cell Biochem. 2013 Aug;380(1-2):57-66.
11. Khara MR, Bodnar YaYa, Saturskaia AS, Pelykh VE; zaiavitel' i patentoobladatel' Tern. gos. med. un-t im. I. Ia. Gorbachevskogo. Pat. 66297 Ukraina, MPK G 09 B 23/28. Sposob modelirovaniia diffuznogo kardioskleroza [Way of modeling of a diffuse cardiosclerosis]. № u 2011 08088; zaiavl. 29.06.11; opubl. 26.12.11, Biul. № 24.
12. Merkulov GA. Kurs patogistologicheskoi tekhniki [Course of patogistologichesky equipment]. Leningrad, RF: Meditsina; 1969. 424 р.
13. Simbirtsev AS. Tsitokiny: klassifikatsiia i biologicheskie funktsii [Cytokines: classification and biological functions]. Tsitokiny i vospalenie. 2004;(2):16–22.
14. Neuhoff S, Moers J, Rieks M, Grunwald T, Jensen A, Dermietzel R, Meier C. Proliferation, differentiation and cytokine secretion of human umbilical cord blood-derived mononuclear cells in vitro. Exp Hematol. 2007 Jul;35(7):1119-31.
15. Haudek SB, Taffet GE, Schneider MD, Mann DL. TNF provokes cardiomyocyte apoptosis and cardiac remodeling through activation of multiple cell death pathways. J Clin Invest. 2007 Sep;117(9):2692-701.
16. Heim M. The Jak-STAT pathway: specific signal transduction from the cell membrane to the nucleus. Eur J Clin Invest. 1996 Jan;26(1):1-12.
17. Caretti A, Morel S, Milano G, Fantacci M, Bianciardi P, Ronchi R, Vassalli G, von Segesser LK, Samaja M. Heart HIF-1alpha and MAP kinases during hypoxia: are they associated in vivo? Exp Biol Med (Maywood). 2007 Jul;232(7):887-94.
18. Katschinski DM. Is there a molecular connection between hypoxia and aging? / D. M. Katschinski. Exp Gerontol. 2006 May;41(5):482-4.
19. Niemi H, Honkonen K, Korpisalo P, Huusko J, Kansanen E, Merentie M, Rissanen TT, André H, Pereira T, Poellinger L, Alitalo K, Ylä-Herttuala S. HIF-1α and HIF-2α induce angiogenesis and improve muscle energy recovery. Eur J Clin Invest. 2014 Oct;44(10):989-99.
