...
首页> 外文期刊>Cellular immunology >The ACE inhibitors enalapril and captopril modulate cytokine responses in Balb/c and C57Bl/6 normal mice and increase CD4(+)CD103(+)CD25(negative) splenic T cell numbers.
【24h】

The ACE inhibitors enalapril and captopril modulate cytokine responses in Balb/c and C57Bl/6 normal mice and increase CD4(+)CD103(+)CD25(negative) splenic T cell numbers.

机译:ACE抑制剂烯丙醇和卡托普尔调节BALB / C和C57BL / 6正常小鼠中的细胞因子反应,并增加CD4(+)CD103(+)CD25(阴性)脾脏T细胞数。

获取原文
获取原文并翻译 | 示例
           

摘要

Increasing evidence implies beneficial effects of angiotensin-converting enzyme (ACE) inhibitors beyond those of their original indications to control hypertension. One of the most attractive non-hemodynamic properties of ACE inhibitors is their ability to regulate cytokine production. The mechanism(s) underlying the role of ACE inhibitors on cytokine synthesis are not well understood but they have traditionally been attributed to the inhibition of angiotensin (Ang) II formation. In fact, it has been extensively demonstrated that ACE inhibitors decrease Ang II-induced production of proinflammatory cytokines and chemokines. However, it is not well described if inhibition of endogenous Ang II generation by ACE inhibitors modulates systemic cytokine production in mice. To verify that, in this work, we investigated the effects of treatment with the ACE inhibitors enalapril and captopril on cytokine synthesis in C57Bl/6 and Balb/c mice. Our results show that enalapril up regulates IL-10 produced by splenocytes from Balb/c and C57Bl/6 mice and captopril increased it only in Balb/c mice. Furthermore, CD4(+)CD103(+) presented increased IL-10 production after enalapril treatment. Enalapril as well as captopril short-term treatment enhanced IL-2 synthesis in Balb/c mice. Besides, enhanced IL-2 and IL-10 levels correlates with increased CD4(+)CD103(+)CD25(negative) T cells numbers in spleens from enalapril-treated mice.
机译:越来越多的证据意味着血管紧张素转换酶(ACE)抑制剂在其原始适应症中的抑制剂的有益作用,以控制高血压。 ACE抑制剂最具吸引力的非血液动力学性质之一是它们调节细胞因子产生的能力。 ACE抑制剂对细胞因子合成作用的机制尚不清楚,但它们传统上归因于血管紧张素(Ang)II形成的抑制。实际上,它已被广泛证明ACE抑制剂降低了致敏细胞因子和趋化因子的产生。然而,如果ACE抑制剂的内源性Ang II产生的抑制调节小鼠的全身细胞因子产生,则不熟悉。为了验证,在这项工作中,我们调查了在C57BL / 6和BALB / C小鼠中对ACE抑制剂Enalapril和Captopril治疗的影响。我们的研究结果表明,Enalapril Up调节由Balb / C的脾细胞产生的IL-10,C57BL / 6小鼠和Captopril仅在Balb / C小鼠中增加它。此外,CD4(+)CD103(+)呈氯氮处理后的IL-10产生增加。 Enalapril以及卡普里尔短期治疗增强了Balb / C小鼠的IL-2合成。此外,增强的IL-2和IL-10水平与脾脏处理小鼠的脾脏中的CD4(+)CD103(+)CD25(负)T细胞数增加相关。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号