Department of Clinical Laboratory, Zhejiang Hospital, Hangzhou, Zhejiang 310013, P.R. China.
Department of Pulmonology, The Children's Hospital of Zhejiang University School of Medicine, Hangzhou, Zhejiang 310052, P.R. China.
Mol Med Rep. 2018 May;17(5):7428-7434. doi: 10.3892/mmr.2018.8730. Epub 2018 Mar 13.
In previous years, studies have shown that Astragalus polysaccharides (APS) can improve cellular immunity and humoral immune function, which has become a focus of investigations. Tumor necrosis factor‑α‑induced protein 8‑like 2 (TIPE2) is a negative regulator of immune reactions. However, the effect and underlying mechanisms of TIPE2 on the APS‑induced immune response remains to be fully elucidated. The present study aimed to examine the role of TIPE2 and its underlying mechanisms in the APS‑induced immune response. The production of nitric oxide (NO) was detected in macrophages in vitro following APS stimulation. In addition, the present study interfered with the expression of TIPE2 in macrophages, and examined the production of cytokines, NO and components of the mitogen‑activate protein kinase (MAPK) signaling pathway following APS stimulation. The results showed that APS was able to activate macrophages by inducing the production of interleukin (IL)‑1β, tumor necrosis factor (TNF)‑α, IL‑6 and NO. Furthermore, RAW264.7 cells were stimulated with APS when TIPE2 was silenced, and it was found that the production of TNF‑α, IL‑6, IL‑1β and NO were upregulated, and the signaling pathway of MAPK was activated. Taken together, these results demonstrated that TIPE2 had an important negative effect on the APS‑induced production of inflammatory cytokines and NO via the MAPK signaling pathway.
在过去的几年中,研究表明黄芪多糖(APS)可以改善细胞免疫和体液免疫功能,这已成为研究的重点。肿瘤坏死因子-α诱导蛋白 8 样蛋白 2(TIPE2)是免疫反应的负调节剂。然而,TIPE2 对 APS 诱导的免疫反应的影响及其潜在机制仍有待充分阐明。本研究旨在探讨 TIPE2 及其在 APS 诱导的免疫反应中的潜在机制的作用。在体外通过 APS 刺激检测巨噬细胞中一氧化氮(NO)的产生。此外,本研究干扰巨噬细胞中 TIPE2 的表达,并检测 APS 刺激后细胞因子、NO 和丝裂原激活蛋白激酶(MAPK)信号通路成分的产生。结果表明,APS 通过诱导白细胞介素(IL)-1β、肿瘤坏死因子(TNF)-α、IL-6 和 NO 的产生来激活巨噬细胞。此外,当沉默 TIPE2 时,用 APS 刺激 RAW264.7 细胞,发现 TNF-α、IL-6、IL-1β 和 NO 的产生上调,并且 MAPK 信号通路被激活。综上所述,这些结果表明 TIPE2 通过 MAPK 信号通路对 APS 诱导的炎症细胞因子和 NO 的产生具有重要的负调控作用。