Role of gut microbiota in the development of pancreatitis-like biochemical changes upon long-term suppression of gastric acid secretion in rats

Sergii Vaka*, Kateryna Dvorshchenko, Alevtina Dranitsina, Lyudmila Ostapchenko

*Korresponderande författare för detta arbete

Forskningsoutput: TidskriftsbidragArtikelVetenskapligPeer review

1 Citeringar (Scopus)

Sammanfattning

Long-term suppression of gastric acid secretion is sometimes associated with development of pancreatitis-like biochemical changes. Few possible mechanisms can be involved: dysbiosis development, hypergastrinemia or direct action of acid suppressants on pancreas. Our aim was to evaluate the role of gut microbiota alterations in the development of pancreatitis-like biochemical changes upon suppression of gastric secretion in rats. Four experimental groups were created with 10 rats in each. One group was a control, while others were injected with acid suppressant omeprazole or multi-strain probiotics preparation or with both compounds simultaneously for 28 days. Alpha-1-antitrypsin and reduced glutathione levels, trypsin, lipase and amylase activities were measured in blood serum and pancreatic tissue with standard biochemical assays. Pancreatic juice proteolytic profile was assessed with contact zymography. Level of Par2 gene mRNA was determined with semi-quantitative RT-PCR. Significant deviation of most studied parameters from the control was observed upon treatment with acid suppressant. Active cationic proteases were identified in pancreatic juice samples of rats upon hypochlorhydria. Most of studied parameters didn't differ from control values upon treatment with multi-strain probiotics preparation. Alterations of gut microbiota have a crucial role in development of pancreatitis-like biochemical changes upon long-term suppression of gastric acid secretion in rats.

OriginalspråkEngelska
Sidor (från-till)386-396
Antal sidor11
TidskriftResearch Journal of Pharmaceutical, Biological and Chemical Sciences
Volym6
Nummer3
StatusPublicerad - 2015
MoE-publikationstypA1 Tidskriftsartikel-refererad

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