Interleukin Expression in the Area damaged by the Development of Abdominal Cavity Adhesions

Shurygina, I. A.; Шурыгин, М. Г.; Rodionova, Lubov; Aushinova, Nataliya; Pharmasyntez,

doi:10.21103/article7(4)_oa4

Cited by 2 publications

(2 citation statements)

References 12 publications

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“…Our main finding is that tissular expression of growth factors during peritoneal wound repair is a biphasic process, with an early phase culminating on day 3 after injury, and a late phase reaching its maximum two weeks after this injury. These results are in line with the expression of proinflammatory cytokines in the abdominal cavity [ 20 ], [ 21 ]. Notably, the second peak at day 14 was usually more pronounced.…”

Section: Discussionsupporting

confidence: 81%

Growth factors in the regulation of reparative response in the presence of peritoneal damage

Shurygina

Шурыгин²,

Rodionova

et al. 2020

Pleura and Peritoneum

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ObjectivesTo study the expression of growth factors in the regulation of tissue repair after peritoneal damage tissue response to peritoneal damage.MethodsExperimental study in 35 male Wistar rats determining the evolution over time of the tissue response to aseptic peritoneal damage. A standardized bowel and peritoneal lesions were created in the right lower quadrant by laparotomy. Then, tissular expression of growth factors was evaluated by multiplex polymerase chain reaction at seven timepoints between 6 h and 30 days, postoperatively.ResultsTissular responses of granulocyte-stimulating factors (Csf2, Csf3), connective tissue growth factor (Ctgf), epidermal growth factors and receptor (Egf, Egfr), fibroblast growth factors (Fgf2, 7 and 10), heparin binding EGF-like growth factor (Hbegf), hepatocyte growth factor (Hgf), insulin-like growth factor-1 (Igf1), mitogenic transforming growth factors (Tgfa, Tgfb1, Tgfbr3), and vascular endothelial growth factor A (Vegfa) were biphasic with a first expression peak at day 3, followed by a more pronounced peak at day 14.ConclusionsWe observed a long-lasting, widespread response of tissular growth factors for at least two weeks after peritoneal damage. To be clinically effective, the prophylaxis of postoperative adhesions might be needed for an extended period of time.

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Section: Discussionsupporting

confidence: 81%

Growth factors in the regulation of reparative response in the presence of peritoneal damage

Shurygina

Шурыгин²,

Rodionova

et al. 2020

Pleura and Peritoneum

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“…Peritoneal adhesions in the animal models were induced by a method developed by the authors that included opening the serous-muscular layer of the caecum with a 1cm cut followed by closing the wound with a Schmieden suture and scarifying a 1.5×1.5 cm area of the parietal peritoneum of the right lateral channel. (11)(12)(13) Experiments were carried out on male 9-month-old Wistar rats (n=80) weighing 220-250 g.…”

Section: Peritoneal Adhesion Simulationmentioning

confidence: 99%

Effect of p38 MAPK Inhibition on Apoptosis Marker Expression in the Process of Peritoneal Adhesion Formation

Shurygina¹,

Aushinova²,

Шурыгин³

2018

IJBM

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Background: Apoptosis, one of the most important mechanisms for maintaining homeostasis, is carried out under both physiological and pathological conditions. The aim of our study was to investigate the expression of markers of apoptosis through caspase-dependent and caspase-independent pathways during the reparative regeneration after serosal injuries of the peritoneum in the context of the prolonged p38 MAPK inhibition. Methods: Peritoneal adhesions in the animal models were induced by a method developed by the authors that included opening the serous-muscular layer of the caecum with a 1cm cut followed by closing the wound with a Schmieden suture and scarifying a 1.5×1.5 cm area of the parietal peritoneum of the right lateral channel. Experiments were carried out on male 9-monthold Wistar rats. When closing the wound, control animals were intraperitoneally administered 3 mL of 0.9% sodium chloride solution (n=40) while experimental group rats were administered slow-release drug Seroguard ® (Pharmasyntez JSC) (n=40). Animals were sacrificed within the period of 2 hours to 30 days post surgery. Expression of apoptosis markers was studied by immunohistochemical (Bcl-2, Bcl-xl) and immunofluorescent (PARP-1) staining. Results: It is interesting that, in cases of the natural regeneration of the peritoneal injury, expression of anti-apoptosis markers at the injury site came in two waves: it was the most pronounced on days 1-3 post surgery while the second peak of activity was observed on day 14. Within this time window, granulation tissue was actively growing and mature connective-tissue vascularized adhesions were being formed. By the end of the observation period (day 30), expression of anti-apoptosis proteins at the injury site became extremely low and a significant reduction in the amount of connective tissue cells was observed. It was found that a prolonged inhibition of the p38 activity resulted in a moderate increase in Bcl-2 expression on days 3-7, and a decrease in the activity on day 14 was followed by another increase in expression by day 30. The Bcl-xl expression was observed 12 hours to 3 days post surgery and then it went down to the minimum. Positive PARP-1 staining observed on days 3 to 30, which reached its maximum on day 14, was also typical of the experimental group. Conclusion: The performed study demonstrated that a prolonged p38 MAPK inhibition in the adhesion formation models results in the activation of fibroblast apoptosis at the reparation site, which, in the authors' opinion, predetermines a significant decrease in the adhesion formation in the experimental group.

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Interleukin Expression in the Area damaged by the Development of Abdominal Cavity Adhesions

Cited by 2 publications

References 12 publications

Growth factors in the regulation of reparative response in the presence of peritoneal damage

Growth factors in the regulation of reparative response in the presence of peritoneal damage

Effect of p38 MAPK Inhibition on Apoptosis Marker Expression in the Process of Peritoneal Adhesion Formation

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