PDF(Pubmed)
Abstract：
Currently, it is known that angiotensin II (AngII) induces inflammation, and an AT1R blockade has anti-inflammatory effects. The use of an AT1 receptor antagonist promotes the inhibition of the secretion of multiple proinflammatory cytokines in macrophages, as well as a decrease in the concentration of reactive oxygen species. The aim of this study was to determine the effect of AT1 receptor gene silencing on the modulation of cytokines (e.g., IL-1β, TNF-α, and IL-10) in THP-1 macrophages and the relation to the gene expression of NF-κB.
METHODS: We evaluated the gene expression of PPAR-γ in THP-1 macrophages using PMA (60 ng/mL). For the silencing, cells were incubated with the siRNA for 72 h and telmisartan (10 µM) was added to the medium for 24 h. After that, cells were incubated during 1 and 24 h, respectively, with Ang II (1 µM). The gene expression levels of AT1R, NF-κB, and cytokines (IL-1β, TNF-α, and IL-10) were measured by RT-qPCR.
RESULTS: We observed that silencing of the AT1 receptor causes a decrease in the expression of mRNA of proinflammatory cytokines (IL-1β and TNF-α), NF-κB, and PPAR-γ.
CONCLUSIONS: We conclude that AT1R gene silencing is an alternative to modulating the production of proinflammatory cytokines such as TNF-α and IL-1β via NF-κB in macrophages and having high blood pressure decrease.
METHODS: We evaluated the gene expression of PPAR-γ in THP-1 macrophages using PMA (60 ng/mL). For the silencing, cells were incubated with the siRNA for 72 h and telmisartan (10 µM) was added to the medium for 24 h. After that, cells were incubated during 1 and 24 h, respectively, with Ang II (1 µM). The gene expression levels of AT1R, NF-κB, and cytokines (IL-1β, TNF-α, and IL-10) were measured by RT-qPCR.
RESULTS: We observed that silencing of the AT1 receptor causes a decrease in the expression of mRNA of proinflammatory cytokines (IL-1β and TNF-α), NF-κB, and PPAR-γ.
CONCLUSIONS: We conclude that AT1R gene silencing is an alternative to modulating the production of proinflammatory cytokines such as TNF-α and IL-1β via NF-κB in macrophages and having high blood pressure decrease.
摘要：
目前,已知血管紧张素II（AngII）会引起炎症，AT1R阻断具有抗炎作用。使用AT1受体拮抗剂促进抑制巨噬细胞中多种促炎细胞因子的分泌，以及活性氧浓度的降低。这项研究的目的是确定AT1受体基因沉默对细胞因子调节的影响（例如，IL-1β,TNF-α,和IL-10）在THP-1巨噬细胞中以及与NF-κB基因表达的关系。
方法：我们使用PMA（60ng/mL）评估了THP-1巨噬细胞中PPAR-γ的基因表达。为了沉默，将细胞与siRNA孵育72小时，并将替米沙坦（10μM）添加到培养基中24小时。细胞在1和24小时内孵育，分别,与AngII（1µM）。AT1R的基因表达水平,NF-κB,和细胞因子(IL-1β，TNF-α,和IL-10）通过RT-qPCR测量。
结果：我们观察到AT1受体的沉默导致促炎细胞因子（IL-1β和TNF-α）mRNA表达的降低，NF-κB,和PPAR-γ。
结论：我们得出结论，AT1R基因沉默是通过NF-κB调节巨噬细胞中TNF-α和IL-1β等促炎细胞因子产生并降低高血压的替代方法。
方法：我们使用PMA（60ng/mL）评估了THP-1巨噬细胞中PPAR-γ的基因表达。为了沉默，将细胞与siRNA孵育72小时，并将替米沙坦（10μM）添加到培养基中24小时。细胞在1和24小时内孵育，分别,与AngII（1µM）。AT1R的基因表达水平,NF-κB,和细胞因子(IL-1β，TNF-α,和IL-10）通过RT-qPCR测量。
结果：我们观察到AT1受体的沉默导致促炎细胞因子（IL-1β和TNF-α）mRNA表达的降低，NF-κB,和PPAR-γ。
结论：我们得出结论，AT1R基因沉默是通过NF-κB调节巨噬细胞中TNF-α和IL-1β等促炎细胞因子产生并降低高血压的替代方法。
