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首页> 外文期刊>Peptides: An International Journal >Effects of central injection of angiotensin-converting-enzyme inhibitor and angiotensin type 1 receptor antagonist on the brain NF-kappaB and AP-1 activities of rats given LPS.
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Effects of central injection of angiotensin-converting-enzyme inhibitor and angiotensin type 1 receptor antagonist on the brain NF-kappaB and AP-1 activities of rats given LPS.

机译：集中注射血管紧张素转换酶抑制剂和血管紧张素1型受体拮抗剂对LPS大鼠脑NF-κB和AP-1活性的影响。

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Angiotensin II (ANG II) activation of the angiotensin type 1 (AT1) receptor facilitates the production of brain interleukin-1beta (IL-1beta) and contributes to the induction of the fever following the intracerebroventricular (i.c.v.) injection of lipopolysaccharide (LPS). The purpose of the present study was to investigate whether proinflammatory transcription factors [nuclear factor-kappaB (NF-kappaB) and activator protein-1 (AP-1)] contribute to the ANG II-dependent production of cytokines within the brain. Interestingly, we found that a single i.c.v. injection of LPS had no effect on NF-kappaB and AP-1 activities in the hypothalamus, hippocampus, and cerebellum at either 1 or 3 h post-injection (except for a decrease in hypothalamic AP-1 activity at 1 h). Furthermore, both an angiotensin-converting-enzyme (ACE) inhibitor and an AT1 receptor antagonist enhanced (rather than reduced) the NF-kappaB and AP-1 activities in the hippocampus and/or cerebellum of rats given LPS. In contrast, an i.c.v. injection of ANG II increased the NF-kappaB activity in the hypothalamus. These results suggest that while "endogenous" ANG II exerts (via AT1 receptors) inhibitory effects on the activation of transcription factors in the brain of rats given LPS, a large dose of exogenous ANG II produces effects opposite to those induced by the presumably small amount of endogenous ANG II released locally by 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 the rat's brain.
机译：血管紧张素1型（AT1）受体的血管紧张素II（ANG II）激活促进脑白介素1beta（IL-1beta）的产生，并在脑室内（i.c.v.）注射脂多糖（LPS）后导致发烧。本研究的目的是研究促炎转录因子[核因子-κB（NF-kappaB）和激活蛋白-1（AP-1）]是否有助于脑内ANG II依赖性细胞因子的产生。有趣的是，我们发现一个单独的i.c.v.注射LPS在注射后1或3小时对下丘脑，海马和小脑的NF-κB和AP-1活性没有影响（除了下丘脑AP-1活性在1 h降低）。此外，血管紧张素转换酶（ACE）抑制剂和AT1受体拮抗剂均可增强（而非降低）LPS大鼠海马和/或小脑中NF-κB和AP-1的活性。相反，i.c.v。注射ANG II可增加下丘脑的NF-κB活性。这些结果表明，“内源性” ANG II对（通过AT1受体）LPS大鼠的大脑中转录因子的激活具有抑制作用，而大剂量的外源性ANG II产生的作用与假定的少量诱导的相反LPS在本地释放的内源性ANG II。我们的研究结果似乎不支持NF-κB和AP-1在ANG II诱导的大鼠脑中LPS诱导的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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