ISSN 2415-3060 (print), ISSN 2522-4972 (online)
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JMBS 2018, 3(3): 224–229

The Influence of Symbiter Multiprobiotics Group on the Gastrin Concentration in Blood Serum and the Microflora Quantitative and Qualitaty Composition of the Rats Stomach and Colon under Prolonged Omeprazole Administration

Pylypenko S., Koval' A.

Hypochlorhydria of gastric juice is the most common pathology of the digestive tract organs, which results in hyperhastrinemia. The latter is a significant factor in the growth and development of tumors in the gastrointestinal tract. The purpose of the article was to investigate the influence of Symbiter's multiprobiotics on the gastrin concentration in serum and the microflora quantitative and qualitative composition of the rats’ stomach and colon under prolonged omeprazole administration. Material and methods. All animals were divided into 4 experimental groups. The first group of animals served as control. During 28 days they were administered one time a day intraperitoneally (in/о) 0,2 ml and perorally (p/o) 0,5 ml of water for injections. The animals of the second group were injected omeprazole and p/o 0,5 ml of water for injections once every twenty-four hours during 28 days. The third group animals were administered omeprazole and the multiprobiotic of "Symbiter® acidophilic" concentrated (Symbiter) once every twenty-four hours during 28 days. The fourth group animals were given omeprazole and multiprobiotic of "Apibact®" (Apibact) once every twenty-four hours during 28 days. Results and discussion. It was set that after 28 days of omeprazole administration, the gastrin concentration in blood serum grew by 3,1 times (p<0,05), that correlates with data other authors about the increase of this hormone secretion after short-time and long-term application of inhibitors of proton pump. The microflora quantitative and quality composition of stomach after 28 days of omeprazole application there were substantial changes. In the control group of rats lactobacilluss (102 CFU/g), fungus of sort of Candida (102 CFU/g), Enterococcus (102 CFU/g), Escherichia coli (103 CFU/g) were sowed from the stomach more often. After 28 days of omeprazole administration in 40% of experimental rats lacto bacteria were not quite sown. Thus, more than in 100 times (p<0,05) colonization of stomach grew by a conditionally-pathogenic microflora and fungus of sort of Candida. On the background of long hypoacidity of the gastric juice, the stomach was inhabited by opportunistic bacteria such as Klebsiella, Staphylococcus aureus, Staphylococcus epidermidis (from hemolysis), whose concentration was significant and was 104-105 CFU/g. The concentration of Enterobacter increased 10 times (p <0.05). Thus, blockade of the proton pump eliminated the effect of bactericidal factor – hydrochloric acid bacteria and created an optimal pH for growth and reproduction of pathogenic microflora and significantly reduced gastric mucosal resistance to colonization by microorganisms. Bacterial gut content study of rats with long hypoacidity of the gastric juice also showed the presence of negative microecological changes that were to imbalance between indicators of pathogenic and normal microflora. The data allowed to conclude that the stomach Klebsiella, Staphylococcus aureus, Staphylococcus epidermidis (from hemolysis) fall migration through intestines upward path. Conclusions. The coadministration of omeprazole and multiprobiotics "Symbiter acidophilus" concentrated and "Apibact" in the rat during the 28 days eliminated the development of dysbiosis in the stomach and colon, which manifested itself in restoring the quantitative and quality composition of the microflora, and also reduced the gastrin concentration in blood serum by 24.9% (p <0.05) and 43.0% (p <0.05), respectively, as compared to the group of rats receiving only omeprazole. Prospects for further research in this direction is to study the microflora quantitative and quality composition in the stomach and large intestine under conditions of prolonged gastric hypochloridrium, as well as the correction of this condition with other multiprobiotic drugs.

Keywords: hypochlorhydria, hiperhastrynemy, dysbiosis, probiotics

Full text: PDF (Ukr) 254K

  1. Brandt Z. Statystycheskye metody analyza nablyudenyy. M: Myr, 1975. 312 s. [Russian]
  2. Glants G. Medyko-byologycheskaya statystyka. M: Praktyka, 1999. 459 s. [Russian]
  3. Stepanov YuM, Latfulina AV. Patogenetychne obgruntuvannya antyoksydantnoyi terapiyi khronichnogo khelikobakternogo gastrytu. Medychni perspektyvy. 2004; IX (4): 47-50. [Ukrainian]
  4. Brunner GH, Lamberts R, Creutzfeldt W. Efficacy and safety of omeprazole in the long-term treatment of peptic ulcer and reflux oesophagitis resistant to ranitidine. Digestion. 1990; 4 (Suppl 1): 64-8.
  5. Burkitt MD, Varro A, Pritchard DM. Importance of gastrin in pathogenesis and treatment of gastric tumors. World J Gastroenterol. 2009; 15 (1): 1-16.
  6. Buttke TM, Sandstrom PA. Redox Regulation of Programmed Cell Death in Lymphocytes. Free Radical Research. 1995; 22 (5): 389-97.
  7. Crum-Cianflone NF. Salmonellosis and the GI Tract: More than Just Peanut Butter. Curr Gastroenterol Rep. 2008: 10 (4): 424-31.
  8. Friis-Hansen L. Achlorhydria is associated with gastric microbial overgrowth and development of cancer: lessons learned from the gastrin knockout mouse. Scandinavian Journal of Clinical and Laboratory Investigation. 2006; 66: 607-22.
  9. Hirschowitz BI. Zollinger-Ellison syndrome: pathogenesis, diagnosis and management. Am J Gastroenterol. 1997; 92 (3): 44-8.
  10. Obszynska JA, Atherfold PA, Nanji M, Glancy D, Santander S, Graham TA, Otto WR, et al. Long-term proton pump induced hypergastrinaemia does induce lineage-specific restitution but not clonal expansion in benign Barrett’s oesophagus in vivo. Gut. 2010; 59: 156-63.
  11. Sipponen P, Harkonen M, Alanko A, Suovaniemi O. Diagnosis of atrophic gastritis from a serum sample. Clin Lab. 2002; 48: 505-15.
  12. Watson SA, Morris TM, McWilliams DF, Harris J, Evans S, Smith A, Clarke PA. Potential role of endocrine gastrin in the colonic adenoma carcinoma sequence. Br J Cancer. 2002; 87 (5): 567-73.