STATE OF THE SMALL INTESTINE AT CHRONIC ENTEROCOLITIS COMBINED WITH STREPTOZOTOCIN-INDUCED DIABETES IN RATS: PATHOBIOCHEMICAL DATA
DOI:
https://doi.org/10.11603/1811-2471.2017.v1.i3.8172Keywords:
chronic entrocolitis, streptozotocin diabetes, morphological changes, free oxygen radicals, tumor necrosis factor alpha, experiment.Abstract
The purpose of our study was to establish the morphological changes of the small intestine wall of animals with diabetes mellitus, chronic enterocolitis and their combination, and to justify the mechanism of their development.
Materials and methods. The study was conducted on 48 white non-linear male rats in accordance with the principles of the European Convention for the Protection of Laboratories. Diabetes mellitus was modeled by a single intraperitoneal administration of streptozotocin to animals aged 2 months, (Sigma Aldrich, USA, at a dose of 60 mg/kg of body weight). Chronic enterocolitis was induced by a free access of animals to 1.0% solution of carrageenan in drinking water for 1 month.
Research results. In the histological examination of the small intestine walls of animals with diabetes were observed significant structural changes. It was noted shortening and flattening the villi of the mucous membrane, indicating their atrophy, while crypt elongation, their depth increased.
There were marked manifestations of the inflammatory process in chronic enterocolitis in rats - widespread infiltration of the mucous membrane and submucosal layer by neutrophilic leukocytes with admixture of lymphocytes, histiocytes, eosinophils.
Experimental animals with chronic enterocolitis on the background of diabetes suffered from a complex pathogenic effect of hyperglycemia and carrageenan, therefore, structural-functional changes of the small intestine were characterized by a large polymorphism.
Conclusions. The analysis of the data gives possibility to conclude that in diabetes mellitus against hyperproduction of free oxygen radicals, structural changes in the small intestine wall of white rats are characterized by the prevalence of dystrophic processes, which can be considered like morphological reflection of enteropathy. In animals with chronic enterocolitis, high concentrations of the tumor necrosis factor determine the morphological picture of inflammation. In chronic enterocolitis combined with diabetes, there is a combination of signs of enteropathy and enteritis with the maximum values of the indicators of free oxygen radicals and tumor necrosis factor alpha and the degree of severity of pathological changes was higher than in the isolated models of these pathological states.
References
Santhanam, S., Rajamanickam, S., Motamarry, A. (2012). Mitochondrial electron transport chain complex dysfunction in the colonic mucosa in ulcerative colitis. Inflamm Bowel Dis, 18,11, 2158-2168.
Rezaie, A., Parker, R.D., & Abdollahi, M. (2007). Oxidative stress and pathogenesis of inflammatory bowel disease: an epiphenomenon or the cause. Dig Dis Sci, 52, 9, 2015-2021.
Alzoghaibi, M.A. (2013). Concepts of oxidative stress and antioxidant defense in Crohn's disease. World J Gastroenterol, 19, 39, 6540-6547.
Sadovnikova, I.V. (2011). Klinicheskie proyavleniya endogennoy intoksikatsii i mehanizmyi metabolicheskoy zaschityi organizma pri hronicheskih gepatitah u detey [Clinical manifestations of endogenous intoxication and mechanisms of metabolic protection of the body in chronic hepatitis in children]. STM, 3, 168-170 [in Ukrainian].
Li, X., Fang, P., & Mai, J. (2013). Targeting mitochondrial reactive oxygen species as novel therapy for inflammatory diseases and cancers. J Hematol Oncol, 6, 1-19.
Myalyuk, O.P., Klishch, I.M., Zayets', V.V., & Marushhak, M.I. (2016). Porushennya enerhozabezpechennya tkanyny pechinky yak odyn iz mekhanizmiv alimentarnoho ozhyrinnya [Violation of energy supply of liver tissue as one of mechanisms of nutritional obesity]. «Naukovi dopovidi NUBiP Ukrayiny» – "Scientific reports of NUBiP of Ukraine", 58. Retrieved from http:// http://nd.nubip.edu.ua/2016_1/2.pdf [in Ukrainian].
West, A.P., Shadel, G.S., & Ghosh S. (2011). Mitochondria in innate immune responses. Nat Rev Immunol, 11, 6, 389-402.
Dada, L.A., & Sznajder, J.I. (2011). Mitochondrial Ca2+ and ROS take center stage to orchestrate TNF-α–mediated inflammatory responses. J Clin Invest, 121, 5, 1683-1685.
Mic, А.А., Mic, F.A., Tatu, С.А., Ionac, М., Ordodi, V.L., & Paunescu, V.L. (2008). Indomethacin inhibits thymic involution in mice with streptozotocininduced diabetes. Artificial organs, 32, 1, 66-70.
Moyana, T.N., & Lalonde, J.M. (1990). Carrageenan-induced intestinal injury in the rat – a model for inflammatory bowel disease. Ann Clin Lab Sci, 20, 6, 420-426.
Gubina-Vakuly`k, G.I., Kolousova, N.G., Ivanenko, Т.О., Gorbach, T.V., Korobchans`ky`j, V.O. Sposib modelyuvannya xronichnogo gastroenterokolitu [Method of modeling chronic gastroenterocolitis]. Patent Ukrayina, № a201014510, 2012 [in Ukrainian].
Reznikov, O. (2003). Zagal`ni ety`chni pry`ncy`py` ekspery`mentiv na tvary`nax [General ethical principles of experiments on animals]. Endokrynolohiya – Еndocrinology, 8,(1), 142-145 [in Ukrainian].
Gouldstejn, Dzh., N'juberi, D., Jechlin, P., Dzhoj, D., Fiori, Ch., & Lifshin, Je. (1984). Rastrovaja jelektronnaja mikroskopija i rentgenovskij analіz [Raster electron microscopy and X-ray analysis]. Moskva: Mir, 162-317 [in Ukrainian].
Bass, D.A., Parce, J.W., Dechatelet, L.R., Szejda, Р., Seeds, М.С., & Thomas, М. (1983). Flow cytometric studies of oxidative product formation by neutrophils: a graded response to membrane stimulation. J Immunol, 130 (4), 1910-1917.
Sennikov, S.V., & Silkov, A.N. (2005). Metody opredelenija citokinov [Methods for the determination of cytokines.]. Citokiny i vospalenie – Cytokines and inflammation, 4, 1, 22-27 [in Ukrainian].
Rebrova, O.Yu. (2002). Statisticheskiy analiz meditsinskih dannyh. Primenenie paketa prikladnyh programm STATISTICA [Statistical analysis of medical data. Application of software package STATISTICA]. M: MediaSfera [in Russian].
Buse, M.G. (2006). Hexosamines, insulin resistance, and the complications of diabetes: current status. Am J Physiol Endocrinol Metab, 290, 1, 1-8.
Drummond, G.R., Selemidis, S., Griendling, К.К, & Sobey, C.G. (2011). Combating oxidative stress in vascular disease: NADPH oxidases as therapeutic targets. Nat Rev Drug Discov, 10, 6, 453-471.
Giacco, F., & Brownlee, М. (2010). Oxidative stress and diabetic complications. Circ Res, 107, 9, 1058-1070.
Drel', V.R. (2010). Osnovni mehanizmy vynyknennja ta rozvytku diabetychnyh uskladnen': rol' nitratyvnogo stresu [The main mechanisms of the emergence and development of diabetic complications: the role of nitrate stress.]. Biologichni Studii' – Biological Studios, 4 (2), 141-158 [in Ukrainian].
Gridneva, S.V. (2003). Rol' okysu azotu i procesiv lipoperoksydacii' u rozvytku hronichnogo nevyrazkovogo kolitu [The role of nitric oxide and lipoperoxidation processes in the development of chronic non-ulcer colitis]. Suchasna gastroenterologija – Modern gastroenterology, 2, 43-46 [in Ukrainian].
Kolisnik, M.I., Kolisnyk, G.V., Nidzjulka, Je., & Vlizlo, V.V. (n. d.) Aktyvni formy kysnju ta i'h rol' u metabolizmi klityn [Active forms of oxygen and their role in cell metabolism]. Instytut biologii' tvaryn UAAN – Institute of animal biology of UAAS. Available at: http://old.inenbiol.com/bt/2009/1/5.pdf
