General regularities and features of apoptosis processes in grain gliosis after tranaious brain injury and abdominal adhesions. Regulation of apoptosis processes by diltiazem

Background. Disturbances in the normal course of apoptosis, its stimulation or blocking, underlie a large number of diseases. Of particular interest is the study of apoptosis in trauma victims, apoptosis-mediated mechanisms of adhesion degradation.

Objective. Identification of general patterns and features of apoptotic processes in cerebral gliosis after traumatic brain injury and abdominal adhesions with regulation of apoptotic processes by diltiazem.

Methods. The work used two experimental models of cicatricial adhesive processes: 1) modeling of severe traumatic brain injury (TBI); 2) modeling of the adhesive process in the abdominal cavity. In the sensorimotor cortex of the brain, the numerical density of neurons and glia was determined, their condition was assessed (staining with hematoxylin and eosin, according to Nissl). Immunohistochemical studies were performed using antibodies to bcl-2 and p53. The number of active forms of the nuclear transcription factor NF-kB was determined by enzyme immunoassay.

Results. TBI was accompanied by a decrease in the numerical density of neurons, an increase in the number of dystrophically and necrobiotically altered neurons, with activation of apoptosis processes in them with high expression of proapoptotic proteins p53. At the same time, the number of astrocytes actively synthesizing apoptosis-blocking proteins bcl-2 increased. Inhibition of apoptosis was also detected in the development of adhesions in the abdominal cavity with pronounced expression of the transcription factor NF-kB. Diltiazem reduced excessive anti-apoptotic activity of NF-kB in peritoneal fibroblasts, contributing to the suppression of cicatricial adhesive processes.

Conclusion. TBI leads to stimulation of apoptosis in neurons of the brain with high expression of p53 and blocking of apoptosis in astrocytes actively synthesizing anti-apoptotic bcl-2 proteins, which contributes to the development of gliosis and microglial scars. Inhibition of apoptosis was also revealed in the development of adhesions in the abdominal cavity by the multiple growth of NF-kB in peritoneal fibroblasts. Glia cells after TBI and peritoneal fibroblasts have a similar direction of apoptosis changes, which provides an anti-apoptotic state in the development of cicatricial adhesive processes: gliosis of the brain, adhesions in the abdominal cavity. Diltiazem reduces apoptotic processes in tissues during adhesion formation.