ROLE OF NO IN SOFT PERIODONTAL TISSUES OF RATS DURING STRESS AND INFLAMMATION

V. Pletnov
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Abstract

Aim. To evaluate the activity of NO-synthase isoforms, the concentration of peroxynitrites and nitrosothiols in the soft tissues of the periodontium of rats under the conditions of modeling chronic stress against the background of lipopolysaccharide-induced inflammation. Methods. Experimental studies were performed on 24 male Wistar rats weighing 190–240 g. The animals were divided into 4 groups: 1 — control, 2 — chronic stress (ChrStr group), animals were kept above water for 1 hour every day for 30 days, 3 — animals that were intraperitoneally injected with 0.4 μg/kg of bacterial LPS of S. typhi (pyrogenal) (LPS group); 4 — animals that were simultaneously simulated chronic stress as in group 2 and administered LPS as in group 3 (ChrStr+LPS). The activity of inducible NO-synthase (iNOS), constitutive NO-synthase (cNOS), the concentration of nitrosothiols (S-NO), and concentration of peroxynitrites of alkali and alkaline earth metals (ONOO) were studied in the homogenate of the periodontal soft tissues of rats. Results. The activity of NOS in the soft periodontal tissues of rats under chronic stress simulation conditions, LPS administration, combined exposure to chronic stress and LPS was increased compared to control group. The concentration of ONOO- in the soft periodontal tissues of rats under chronic stress simulation conditions, LPS administration, combined exposure to chronic stress and LPS was increased compared to the control group. The concentration of nitrosothiols in the soft periodontal tissues of rats under the conditions of chronic stress simulation, LPS administration, combined exposure to chronic stress and LPS was decreased compared to the control group. Conclusions. The combined effect of bacterial lipopolysaccharide and chronic stress leads to increased production of nitrogen monoxide from inducible NO-synthase and elevates concentration of reactive forms of nitrogen, which creates possibility for development of nitrosative stress in the soft periodontal tissues.
NO在大鼠牙周软组织应激和炎症过程中的作用
目标在脂多糖诱导的炎症背景下,评估慢性应激模型条件下大鼠牙周组织中NO合酶亚型的活性、过氧亚硝酸盐和亚硝基硫醇的浓度。方法。对24只体重190–240 g的雄性Wistar大鼠进行了实验研究。将动物分为4组:1组为对照组,2组为慢性应激组(ChrStr组),每天在水上饲养1小时,持续30天;3组为腹腔注射0.4μg/kg伤寒杆菌LPS(热原)(LPS组);4-与第2组一样同时模拟慢性应激并与第3组一样给予LPS(ChrStr+LPS)的动物。研究了大鼠牙周软组织匀浆中诱导型一氧化氮合酶(iNOS)、组成型一氧化氮合合酶(cNOS)的活性、亚硝基硫醇(S-NO)的浓度以及碱金属和碱土金属过氧亚硝酸盐(ONOO)的浓度。后果与对照组相比,在慢性应激模拟条件下、LPS给药、慢性应激和LPS联合暴露下,大鼠牙周软组织中NOS活性增加。与对照组相比,在慢性应激模拟条件下、LPS给药、慢性应激和LPS联合暴露下,大鼠软牙周组织中ONOO-的浓度增加。与对照组相比,在慢性应激模拟、LPS给药、慢性应激和LPS联合暴露条件下,大鼠牙周软组织中亚硝基硫醇的浓度降低。结论。细菌脂多糖和慢性应激的联合作用导致诱导型一氧化氮合酶产生的一氧化氮增加,并提高反应性氮的浓度,这为软牙周组织中亚硝化应激的发展创造了可能性。
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