Оценка взаимодействия фактора роста нервов и тучных клеток при интерстициальном цистите/синдроме болезненного мочевого пузыря в эксперименте

Abstract

to evaluate the level of nerve growth factor (NGF) in the blood and urine and mast cell infiltration of the bladder wall in a model of interstitial cystitis/bladder pain syndrome (IC/BPS) and to analyze their relationships. IC/BPS modeling was performed on 38 female rabbits, which were divided into 4 groups. In the group 1, IC/BPS was simulated by an instillation of 70% alcohol into the bladder, while in group 2 and 3 animals own urine and normal saline were injected into the bladder wall. The group 4 consisted of intact animals. The NGF level was determined by ELISA. To determine the concentration of mast cell in tissues, each cross-section was divided into 10 sections. The severity of mast cell infiltration was evaluated in each area using the following scale: 0 - no mast cells; 1 - less than 20 cells; 2 - 20-45 cells; 3 - more than 45 cells. The points of all 10 areas were added up, divided by 30 (the maximum possible score) and multiplied by 100. An increase in the NGF level in the blood and urine was seen in different models of IC/BPS, but it was significantly more pronounced in the group 2 (toxic model). Mast cells were determined only in the group 1 (0.25+/-0.707) and 2 (14,200+/-5,796). In animals with the urinary toxicity model, mast cell activity was significantly higher in comparison with those in the model with an instillation of 70% alcohol (p<0.001). The level of NGF in blood and urine correlated in different directions. Mast cell proliferation and activation was determined in case of impairment of the bladder wall integrity by the injection of urine. Our animal model of IC/BPS, which was created by instillation of 70% alcohol into the bladder and the injection of urine into the bladder wall, showed an increase in the level of NGF in urine and blood and the concentration of mast cells. These findings, as well as relationship between these values indicate the development of neuroimmune inflammation in this pathological condition. Considering the involvement of many factors in the pathogenesis of this syndrome, further researches are required.