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首页> 外文期刊>American Journal of Physiology >Are transcription factors NF-kappaB and AP-1 involved in the ANG II-stimulated production of proinflammatory cytokines induced by LPS in dehydrated rats?
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Are transcription factors NF-kappaB and AP-1 involved in the ANG II-stimulated production of proinflammatory cytokines induced by LPS in dehydrated rats?

机译：在脱水大鼠中，转录因子NF-κB和AP-1是否参与ANG II刺激的LPS诱导的促炎细胞因子的产生？

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We recently reported an involvement of ANG II and the ANG II type 1 (AT1) receptor in the hepatic expression of IL-1beta induced in dehydrated rats by LPS. Here, we first confirmed that ANG II and AT1 receptors contribute to the LPS-induced increase in the splenic concentration of IL-1beta in dehydrated rats. We then investigated whether ANG II contributes to IL-1 production through a modulating effect on the activation of proinflammatory transcription factors (NF-kappaB and AP-1) that is induced in the dehydrated rat's liver and spleen by intravenous injection of LPS. Surprisingly, LPS markedly increased the hepatic activation of NF-kappaB, an effect that was significantly enhanced (rather than reduced) by pretreatment with an ANG-converting-enzyme (ACE) inhibitor or AT1-receptor antagonist. Furthermore, the same ACE inhibitor and AT1-receptor antagonist each increased the resting NF-kappaB activity in the liver and spleen, although they had no effect on the LPS-induced splenic expression of NF-kappaB. Both hepatic and splenic AP-1 expressions were enhanced by LPS. This response was significantly augmented by pretreatment with the AT1-receptor antagonist (but not with the ACE inhibitor) in the spleen, while in the liver, neither drug had any effect. These results suggest that the endogenous ANG II or AT1 receptor suppresses the activation of hepatic or splenic transcription factors in dehydrated rats given LPS. Our results seem not to support the idea that NF-kappaB and AP-1 play key roles in the ANG II-induced enhancement of the production of proinflammatory cytokines that is induced by LPS in dehydrated rats.
机译：最近，我们报道了ANG II和ANG II 1型（AT1）受体参与了LPS诱导的脱水大鼠肝脏IL-1beta的肝表达。在这里，我们首先确认ANG II和AT1受体有助于LPS诱导的脱水大鼠脾脏中IL-1β脾脏浓度的增加。然后，我们调查了ANG II是否通过对脱水大鼠肝脏和脾脏通过静脉注射LPS诱导的促炎转录因子（NF-κB和AP-1）活化的调节作用来促进IL-1的产生。出人意料的是，LPS显着增加了NF-κB的肝激活，这种作用通过用ANG转化酶（ACE）抑制剂或AT1-受体拮抗剂进行预处理而得到了显着增强（而不是降低）。此外，尽管它们对LPS诱导的NF-kappaB的脾脏表达无影响，但相同的ACE抑制剂和AT1-受体拮抗剂各自增加了肝脏和脾脏中的静息NF-kappaB活性。 LPS增强了肝和脾AP-1的表达。通过在脾脏中使用AT1受体拮抗剂（但不使用ACE抑制剂）进行预处理，可以大大增强这种反应，而在肝脏中，这两种药物都没有任何作用。这些结果表明内源性ANG II或AT1受体抑制了给予LPS的脱水大鼠肝或脾转录因子的激活。我们的结果似乎不支持NF-κB和AP-1在ANG II诱导的LPS诱导的脱水大鼠中促炎性细胞因子产生的增强中起关键作用的想法。

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