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首页> 外文期刊>Ukrainian Biochemical Journal >Role of peripheral dopaminergic system in the pathogenesis of experimental colitis in rats
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Role of peripheral dopaminergic system in the pathogenesis of experimental colitis in rats

机译：外周多巴胺能系统在大鼠实验性结肠炎发病中的作用

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Dopamine (DA) is produced and released by immune cells. Recent data pointed to DA as a key mediator between the nervous and immune systems. In the present study we tested the hypothesis that peripheral dopaminergic system plays a negative role in ulcerative colitis pathogenesis via the effect on activity of peripheral blood phagocytes. The study was conducted on male Wistar rats (170-200 g). The peripheral dopaminergic system was destroyed by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) injection (20 mg/kg, s.c., 4 times every 2 h). Colitis was induced by 0.1 ml 6% iodoacetamide enema. Rats were subjected to autopsy on the 18supth/sup day. We found that MPTP-treated rats had decreased levels of tyrosine hydroxylase, rate-limiting enzyme of DA synthesis, in colon but not in brain. The number and activity of colonic and peripheral blood granulocytes did not significantly differ in saline- and MPTP-treated rats with colitis. The decreased ROS production by monocytes; increased 1.8-fold the number of CD69 (an early activation marker) positive monocytes and 6-fold intensity of CD69 surface expression were observed in MPTP-treated rats vs. saline-treated rats during colitis. The CD14 (the endotoxin coreceptor of phagocytes) surface expression was 2-fold increased in MPTP-treated rats without colitis, but significantly decreased in both saline- and MPTP-treated rats with colitis. We showed for the first time that the destruction of peripheral dopaminergic neurons leads to the improvement of morphological signs of experimental colitis, which might be through the regulatory effect of dopaminergic system on monocytes phenotype and their respiratory burst activity.
机译：多巴胺（DA）由免疫细胞产生和释放。最近的数据表明，DA是神经系统和免疫系统之间的关键介体。在本研究中，我们测试了以下假设：外周多巴胺能系统通过对外周血吞噬细胞活性的影响在溃疡性结肠炎的发病机理中起负作用。该研究是在雄性Wistar大鼠（170-200 g）上进行的。外周多巴胺能系统被1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）注射（20 mg / kg，皮下注射，每2小时4次）破坏。 0.1 ml 6％碘乙酰胺灌肠诱发结肠炎。在第18天对大鼠进行尸检。我们发现，用MPTP处理的大鼠结肠中而非大脑中的酪氨酸羟化酶（DA合成的限速酶）水平降低。盐水和MPTP治疗的结肠炎大鼠结肠和外周血粒细胞的数量和活性没有显着差异。单核细胞产生的ROS减少;在结肠炎期间，MPTP处理的大鼠与生理盐水处理的大鼠相比，CD69（早期激活标记）阳性单核细胞数目增加了1.8倍，而CD69表面表达的强度增加了6倍。在没有结肠炎的MPTP治疗的大鼠中，CD14（吞噬细胞的内毒素共受体）表面表达增加了2倍，而在盐水和MPTP治疗的结肠炎大鼠中，CD14（吞噬细胞的内毒素核心受体）表面表达增加了2倍。我们首次表明，外周多巴胺能神经元的破坏导致实验性结肠炎的形态学症状改善，这可能是由于多巴胺能系统对单核细胞表型及其呼吸爆发活性的调节作用所致。

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