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首页> 外文期刊>Ukrainian Biochemical Journal >Role of AP-1 transcriptional factor in development of oxidative and nitrosative stress in periodontal tissues during systemic inflammatory response
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Role of AP-1 transcriptional factor in development of oxidative and nitrosative stress in periodontal tissues during systemic inflammatory response

机译：AP-1转录因子在全身炎症反应过程中牙周组织氧化和亚硝化应激发展中的作用

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Chronic systemic inflammatory response syndrome (SIRS) underlies many diseases (sepsis, atherosclerosis, diabetes mellitus). According to research data of recent years the key role in the development of SIRS is played by the activation of various nuclear transcription factors. The work was aimed at studying the role of such transcription factor as activator protein 1 (AP-1) in the development of oxidative and nitrosative stress in soft periodontal tissues during chronic systemic inflammatory response (SIRS). The experiment was carried out on 24 the Wistar rats. We induced SIRS by bacterial lipopolysaccharide of Salmonella typhi (0.4?μg/kg) intraperitoneal injection. We studied changes in the functioning of the nitric oxide (NO) cycle, the production of superoxide anion radical (Osub2/subsup?-/sup) and the activity of antioxidant enzymes in soft periodontal tissues homogenate. We used SR11302 as an Ap-1 inhibitor (15 mg/kg) for 2 months. We established that during the SIRS modeling, the activity of antioxidant enzymes in soft periodontal tissues decreased with a simultaneous increase in the production of Osub2/subsup?-/sup. SIRS elevated the production of NO by inducible NO-synthase (iNOS) and nitrite reductases. The nonoxidative cleavage of L-arginine under this condition was also increased. The concentration of peroxynitrite (ONOOsup–/sup) was shown to be elevated more than 2-fold. The inhibition of AP-1 by SR11302 normalized the functional state of the NO cycle, reduced Osub2/subsup?-/sup production and restored the activity of antioxidant enzymes. In this way, under SIRS conditions, “vicious circle” of ONOOsup–/sup formation is formed. SIRS in soft periodontal tissues poses a threat of oxidative and nitrosative stress development. Usage of AP-1 activation inhibitor SR11302 breaks “vicious circle” of ONOOsup–/sup formation.
机译：慢性全身炎症反应综合征（SIRS）是许多疾病（败血症，动脉粥样硬化，糖尿病）的基础。根据近年来的研究数据，SIRS发展中的关键作用是各种核转录因子的激活。这项工作的目的是研究诸如转录因子激活蛋白1（AP-1）在慢性全身性炎症反应（SIRS）期间牙周组织氧化应激和亚硝化应激发展中的作用。实验是对24只Wistar大鼠进行的。我们通过伤寒沙门氏菌细菌脂多糖（0.4？μg/ kg）腹腔注射诱导SIRS。我们研究了软性牙周组织中一氧化氮（NO）循环功能，超氧阴离子自由基（O 2 ？-）的产生以及抗氧化酶活性的变化。组织匀浆。我们使用SR11302作为Ap-1抑制剂（15 mg / kg）2个月。我们建立了在SIRS建模过程中，软牙周组织中抗氧化酶的活性降低，同时O 2 ？-的产量增加的趋势。 SIRS通过诱导型NO合酶（iNOS）和亚硝酸盐还原酶提高了NO的产生。在这种条件下，L-精氨酸的非氧化裂解也增加了。过氧亚硝酸盐（ONOO – ）的浓度升高了2倍以上。 SR11302对AP-1的抑制作用使NO循环的功能状态正常化，减少了O 2 α-的产生，并恢复了抗氧化酶的活性。这样，在SIRS条件下，形成了ONOO – 形成的“恶性循环”。软牙周组织中的SIRS构成了氧化和亚硝化应激发展的威胁。 AP-1激活抑制剂SR11302的使用打破了ONOO – 形成的“恶性循环”。

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