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首页> 外文期刊>Life sciences >Inhibition by triptoquinone-A of LPS- and IL-1 beta-primed induction of NO synthase in rat thoracic aorta.
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Inhibition by triptoquinone-A of LPS- and IL-1 beta-primed induction of NO synthase in rat thoracic aorta.

机译:雷公藤醌-A对大鼠胸主动脉中LPS-和IL-1β引发的NO合酶的抑制作用。

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摘要

We investigated the effect of triptoquinone-A (TQA), an active principal of Triptergium wilfordii, on the induction of nitric oxide synthase (NOS) promoted by endotoxin (LPS) and interleukin-1 beta (IL-1 beta). Prophylactic application of TQA selectively prevented LPS-primed initiation of L-arginine (Arg)-induced relaxation, and cGMP formation of rat thoracic aorta, and LPS-stimulated nitrite production by cultured aortic smooth muscle cells, which appear to be mediated by NOS expressed by LPS in vascular smooth muscle. TQA also prevented IL-1 beta-triggered initiation of Arg-induced relaxation and nitrite accumulation. These results suggest that TQA prevents LPS-or IL-1 beta-promoted induction of NOS in vascular smooth muscle, thus inhibiting development of Arg-induced vasorelaxation.
机译:我们调查了雷公藤的活性成分雷公藤醌A(TQA)对内毒素(LPS)和白介素1β(IL-1 beta)促进的一氧化氮合酶(NOS)的诱导作用。 TQA的预防应用选择性地阻止了LPS引发的L-精氨酸(Arg)诱导的松弛,大鼠胸主动脉的cGMP形成以及培养的主动脉平滑肌细胞的LPS刺激的亚硝酸盐生成,这似乎是由NOS介导通过LPS在血管平滑肌中的作用。 TQA还阻止了IL-1β触发的Arg诱导的松弛和亚硝酸盐积累。这些结果表明,TQA阻止了LPS或IL-1β促进的血管平滑肌NOS诱导,从而抑制了Arg诱导的血管舒张的发展。

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