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Influence of Angiotensin II on cell viability and apoptosis in rat renal proximal tubular epithelial cells in in vitro studies

机译:血管紧张素II对大鼠肾近侧管状上皮细胞细胞活力和细胞凋亡的影响

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Introduction: Angiotensin II (Ang II) is multifunctional peptide that plays an important role in blood pressure regulation and maintenance electrolyte homeostasis. It shows biological effects by activating two main receptors: AT 1 and AT 2 . The aim of the present work was to investigate the effect of Ang II on NRK-52E cells in in vitro studies. Furthermore, an attempt was made to determine the effectiveness of the AT 1 and AT 2 receptor blocker activity (respectively, losartan and PD123319). Methods: The study was carried out using adherent NRK-52E cell line. Immunofluorescence and Western Blot method were used to confirm the presence of AT 1 and AT 2 receptors in the cells. The SRB and MTT tests showed decrease in the viability of NRK-52E cells incubated with Ang II in comparison to the control (without Ang II). Results: The blockade of the AT 1 receptor caused an increase in cell viability in comparison to cells incubated with Ang II only. The blockade of AT 2 receptor also triggered statistically significant increase in cell viability in comparison with cells only exposed to Ang II. Combined administration of blockers for both receptors (losartan and PD123319) decreased Ang II cytotoxicity against NRK-52E cell line. The apoptosis was only observed in cells incubated with Ang II in comparison with control cells. However, simultaneous use of both blockers caused statistically significant decrease in apoptosis. Conclusions: The result of our study indicates that Ang II causes damaging effect on NRK-52E cells by directing them to programmed cell death. It seems that not only does the AT 2 receptor itself play an important role in the induction of apoptosis, but also its interaction with AT 1 receptor does as well.
机译:简介:血管紧张素II(Ang II)是多官能肽,其在血压调节和维护电解质稳态中起重要作用。它通过激活两个主要受体显示生物效应:在1和2时。本作本作的目的是探讨Ang II对体外研究中NRK-52E细胞的影响。此外,试图确定在1和2受体阻滞剂活性的有效性(分别,氯沙坦和PD123319)。方法:使用粘附的NRK-52E细胞系进行该研究。使用免疫荧光和蛋白质印迹法用于确认细胞中的1和2个受体的存在。与对照(没有Ang II),SRB和MTT试验显示与Ang II孵育的NRK-52E细胞的活力降低。结果:与仅与Ang II孵育的细胞相比,在1个受体的阻断导致细胞活力增加。与仅暴露于Ang II的细胞相比,在2个受体的阻断也引发了细胞活力的统计学显着增加。对BORK-52E细胞系的综合施用阻滞剂(氯沙坦和PD123319)降低了ANG II细胞毒性。与对照细胞相比,仅在与Ang II孵育的细胞中观察到细胞凋亡。然而,同时使用两种阻断剂导致细胞凋亡的统计学显着降低。结论:我们的研究结果表明,Ang II通过将它们指导对细胞死亡引起对NRK-52E细胞的破坏性影响。似乎在2个受体本身不仅在诱导细胞凋亡中发挥着重要作用,而且其与1个受体的相互作用也是如此。

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