Rubiadin-1-methyl Ether 的抗炎作用具有免疫调节作用的证据。,Mediators of Inflammation

当前位置： X-MOL 学术 › Mediat. Inflamm. › 论文详情

Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)

Rubiadin-1-methyl Ether 的抗炎作用具有免疫调节作用的证据。
Mediators of Inflammation ( IF 4.4 ) Pub Date : 2019-11-03 , DOI: 10.1155/2019/6474168
Eduarda Talita Bramorski Mohr ₁ , Marcus Vinicius Pereira Dos Santos Nascimento ₁ , Júlia Salvan da Rosa ₁ , Guilherme Nicácio Vieira ₁ , Iara Fabricia Kretzer ₁ , Louis Pergaud Sandjo ₂ , Eduardo Monguilhott Dalmarco ₁

Affiliation

背景。尽管有最新的治疗进展，但尚未发现用于处理急性肺损伤等危急情况的有效治疗方法。这种情况可能由肺部感染、败血症、多发性创伤或休克引起，这对重症监护医学来说是一个重大挑战。为了寻求更好地应对这一挑战的方法，科学界最近非常关注源自具有抗炎和免疫调节作用的天然产物的小分子。目标。在此背景下，我们使用LPS 诱导的 RAW 264.7 巨噬细胞体外模型和体内LPS诱导的急性肺损伤（ALI）模型。方法。用该化合物预处理巨噬细胞并由LPS（ 1μg /mL）诱导。24 小时后，我们使用上清液评估细胞毒性、NOx 和 IL-6、IL-1 β和 TNF - α水平，以及该化合物对巨噬细胞凋亡的影响。接下来，将该化合物给予 LPS (5 mg/kg) 诱导的急性肺损伤 (ALI) 小鼠，并在 12 小时后使用支气管肺泡灌洗液 (BALF) 分析促炎和抗炎参数。结果。Rubiadin-1-methyl ether 能够抑制体外试验中研究的促炎参数（NOx、IL-6 和 IL-1 β)，同时增加巨噬细胞凋亡率。在体内实验中，这种化合物能够减少白细胞浸润；流体泄漏；氮氧化物；IL-6、IL-12p70、IFN- γ、TNF - α和 MCP-1 水平；和 MPO 活动。此外，Rubiadin-1-methyl ether 增加了支气管肺泡灌洗液 (BALF) 中的 IL-10 水平。结论。这些发现支持 Rubiadin-1-methyl ether 具有重要的抗炎活性的证据，并具有免疫调节作用的证据。

"点击查看英文标题和摘要"

Evidence That the Anti-Inflammatory Effect of Rubiadin-1-methyl Ether Has an Immunomodulatory Context.

Background. In spite of the latest therapeutic developments, no effective treatments for handling critical conditions such as acute lung injuries have yet been found. Such conditions, which may result from lung infections, sepsis, multiple trauma, or shock, represent a significant challenge in intensive care medicine. Seeking ways to better deal with this challenge, the scientific community has recently devoted much attention to small molecules derived from natural products with anti-inflammatory and immunomodulatory effects. Aims. In this context, we investigated the anti-inflammatory effect of Rubiadin-1-methyl ether isolated from Pentas schimperi, using an in vitro model of RAW 264.7 macrophages induced by LPS and an in vivo model of acute lung injury (ALI) induced by LPS. Methods. The macrophages were pretreated with the compound and induced by LPS (1 μg/mL). After 24 h, using the supernatant, we evaluated the cytotoxicity, NOx, and IL-6, IL-1β, and TNF-α levels, as well as the effect of the compound on macrophage apoptosis. Next, the compound was administered in mice with acute lung injury (ALI) induced by LPS (5 mg/kg), and the pro- and anti-inflammatory parameters were analyzed after 12 h using the bronchoalveolar lavage fluid (BALF). Results. Rubiadin-1-methyl ether was able to inhibit the pro-inflammatory parameters studied in the in vitro assays (NOx, IL-6, and IL-1β) and, at the same time, increased the macrophage apoptosis rate. In the in vivo experiments, this compound was capable of decreasing leukocyte infiltration; fluid leakage; NOx; IL-6, IL-12p70, IFN-γ, TNF-α, and MCP-1 levels; and MPO activity. In addition, Rubiadin-1-methyl ether increased the IL-10 levels in the bronchoalveolar lavage fluid (BALF). Conclusions. These findings support the evidence that Rubiadin-1-methyl ether has important anti-inflammatory activity, with evidence of an immunomodulatory effect.

更新日期：2019-11-03

点击分享查看原文

点击收藏

公开下载

阅读更多本刊新发论文本刊介绍/投稿指南