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Regulation of angiotensin II receptors levels during rat induced pulpitis.

机译:大鼠诱发牙髓炎期间血管紧张素II受体水平的调节。

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A change in the microcirculatory hemodynamic is one of the most important events in inflammation. In the dental pulp, which is a connective tissue surrounded by a mineralized dentine substrate, disturbance in the blood flow as well as plasma extravasation may increase the pulp pressure and cause local ischemia. The octapeptide angiotensin II (AngII) regulates vascular tone and stimulates the release of pro-inflammatory cytokines by acting through the AT(1) and AT(2) receptors. The AT(1) receptor is responsible for the classical effects of AngII. The AT(2) receptor is involved in other effects, such as vasodilation. Therefore, we aimed to evaluate the role of AT(1) and AT(2) receptors on the pulpal inflammation. The pulp tissue was mechanically exposed and after different periods the teeth were extracted and submitted to histopathological and RT-PCR analyses. The histological sections showed a number of congested and dilated blood vessels associated with a notable presence of inflammatory cells. RT-PCR data revealed that the AT(1) receptor was down-regulated at 24 h after the pulp exposure. The AT(2) receptor expression was up-regulated by a 9-hour period, and then decreased between 12- and 24-hour periods. It was demonstrated that the renin-angiotensin system plays an important role in the pulpal inflammation, with regulation of AngII receptor levels.
机译:微循环血流动力学的变化是炎症中最重要的事件之一。在由矿化的牙本质基质包围的结缔组织牙髓中,血流紊乱以及血浆外渗可能会增加牙髓压力并引起局部缺血。八肽血管紧张素II(AngII)通过AT(1)和AT(2)受体起作用,调节血管紧张度并刺激促炎性细胞因子释放。 AT(1)受体负责AngII的经典作用。 AT(2)受体还参与其他作用,例如血管舒张。因此,我们旨在评估AT(1)和AT(2)受体对牙髓炎症的作用。机械地暴露牙髓组织,并在不同时期后拔出牙齿,并进行组织病理学和RT-PCR分析。组织学切片显示大量血管充血和扩张,并伴有明显的炎症细胞。 RT-PCR数据显示,牙髓暴露后24小时,AT(1)受体被下调。 AT(2)受体表达在9小时内上调,然后在12小时和24小时内下降。已经证明,肾素-血管紧张素系统在牙髓炎症中起重要作用,并调节AngII受体水平。

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