Markers of Inflammation in Rats Under Toxic Injury Against Dietary Protein Deficiency

Abstract

The paper presents studies of biomarkers of the development of inflammatory reactions in the blood serum of rats under the conditions of toxic damage with acetaminophen against the background of dietary protein deficiency. The animals consumed a semi-synthetic diet during the experiment according to the recommendations of the American Institute of Nutrition. In order to simulate alimentary protein deprivation, rats received a low-protein diet containing 1/3 of the standard daily protein requirement daily for 28 days. The animals were modeled acute toxic damage with acetaminophen after four weeks of experimental diet. The administration of the toxin was carried out at doses of 1250 mg/kg animal body weight in suspension in 2 % starch gel solution once a day for 2 days by gavage. Determination of the level of C-reactive protein, procalcitonin, tumor necrosis factor-alpha, interleukin-6 in the blood serum of rats was carried out by the method of immunoenzymatic analysis. We have established that toxic damage by the drug xenobiotic - acetaminophen against the background of dietary protein deficiency is accompanied by a maximum increase in the level of C-reactive protein (15.5 times) and procalcitonin (10 times) in the blood serum of rats compared to the control value, which can be considered as prognostic biomarkers of the systemic inflammatory reaction under these experimental conditions. At the same time, under these experimental conditions, hyperproduction of tumor necrosis factor-alpha and interleukin-6 was registered in the blood serum of experimental groups of rats with maximum values when toxic doses of acetaminophen were administered to protein-deficient animals, which is consistent with changes in the level of C-reactive protein and procalcitonin. The fact we found makes it possible to assume that dietary protein deprivation increases the production of TNF-α and IL-6 as pro-inflammatory mediators in toxic liver damage, thus inducing primary damage to liver parenchymal cells..