IMMUNOMODULATING EFFECT OF PRP THERAPY IN EXPERIMENTAL ACUTE PERITONITIS

Abstract

The aim of the work: to establish the effect of platelet-rich plasma (PRP) on the level of oxidative stress and phagocytic activity of neutrophils in modeling experimental peritonitis in rats.

Material and Methods. The experimental study was conducted on sexually mature white male Wistar rats weighing 200–220 g, randomly selected from the vivarium of the I. Horbachevsky Ternopil National Medical University. The acute peritonitis model was reproduced by intraperitoneal injection of 10 % fecal suspension. 24 hours after the induction of the pathological process, the animals of the main group were injected with PRP. Biomarker evaluation was performed on the 1st, 4th, 7th and 10th days of the experiment. The dynamics of changes in endotoxicosis indicators, immune response, oxidative stress and phagocytic activity of neutrophil granulocytes were studied. All experimental procedures were performed in accordance with the ethical principles approved by the First National Congress on Bioethics and in accordance with the requirements of the European Convention for the Protection of Vertebrate Animals Used for Experimental and Other Scientific Purposes. Statistical processing of the obtained data was carried out using the Statistica 10.0 software (StatSoft Inc., USA).

Results. The use of platelet-rich plasma in experimental peritonitis contributes to a decrease in the level of oxidative stress and the restoration of neutrophil phagocytic activity. The dynamics of CD8⁺ T-lymphocytes in the process of the development of experimental peritonitis was characterized by an initial increase in their number in the acute period of the disease. It was noted that a further decrease in the level of CD8⁺ cells at later stages of observation may indicate the depletion of the functional reserves of T-killers, suppression of the cellular component of immunity and a decrease in the body's ability to effectively control the infectious process. A stable increase in the number of CD22⁺ B-lymphocytes throughout the entire period of the experiment indicates a long-term activation of the humoral component of immunity. The use of platelet-rich plasma (PRP) had a pronounced regulatory effect on the course of the immune response. A decrease in the levels of CD4⁺ and CD22⁺ cells indicates the suppression of excessive activation of both T-helper and humoral components of immunity, which reduces the risk of developing immunopathological reactions and damage to target organs. A simultaneous increase in the content of CD8⁺ T-lymphocytes and normalization of the CD4⁺/CD8⁺ ratio indicate the restoration of the cytotoxic function of the immune system and an increase in the body's ability to effectively eliminate pathogens. The obtained experimental results confirm the presence of a pronounced multicomponent therapeutic effect of platelet-rich plasma (PRP) in the modeling of acute peritonitis in rats.

Conclusions. The analysis demonstrated the systemic effect of PRP on the key pathogenetic links of the disease course – oxidative, immune and metabolic disorders. Acute peritonitis is accompanied by a significant increase in the levels of reactive oxygen species, medium-weight molecules and circulating immune complexes, which indicates excessive oxidative and endotoxic load. These processes contribute to damage to cellular structures, increased inflammatory response and progression of endogenous intoxication. PRP exhibits a complex anti-inflammatory, antioxidant and immunomodulatory effect in experimental peritonitis. Its use helps restore the balance of cellular and humoral immune response, reduce the level of systemic intoxication, and improve the functional state of the liver as a target organ. The results of the study indicate the feasibility of using PRP as a promising therapeutic agent as part of the complex treatment of peritonitis in order to reduce the manifestations of immunopathological reactions, prevent complications, and improve clinical prognosis.

Received: 05.01.2025 | Revised: 26.01.2026 | Accepted: 23.02.2026