Department of Oral Biochemistry, Asahi University School of Dentistry Mizuho, Gifu 501-0296, Japan.
Department of Oral and Maxillofacial Surgery, Asahi University School of Dentistry, Mizuho, Gifu 501-0296, Japan.
J Oral Biosci. 2023 Dec;65(4):386-394. doi: 10.1016/j.job.2023.08.001. Epub 2023 Aug 16.
We evaluated the immune-modulatory effects of Chinese propolis (CP) and its major constituent, caffeic acid phenethyl ester (CAPE), on the cytokine production of anti-CD3 antibody-stimulated mouse spleen cells.
Mouse spleen cells stimulated by anti-CD3 monoclonal antibody were co-cultured with CP, CAPE, and HC030031, a specific antagonist of the TRPA1 Ca-permeable cation channel. Cytokine production was assayed by enzyme-linked immunosorbent assay. Interleukin (IL)-2 mRNA expression was examined by reverse transcription-quantitative polymerase chain reaction.
In stimulated spleen cells treated with 1/16,000 CP diluent, IL-2 production was markedly enhanced, while IL-4 and IL-10 productions were not significantly affected. In contrast, interferon (IFN)-γ, IL-6, and IL-17 productions were markedly reduced. These effects of CP were reproduced by the CAPE treatment. A time-course observation demonstrated that, compared to control cells, IL-2 mRNA expression and production were significantly enhanced in the spleen cells stimulated by CAPE; however, IL-2 production was markedly delayed compared to that in the untreated control cells. The enhancement of IL-2 production by CAPE was scarcely alleviated by the addition of HC030031. These effects of CAPE upon IL-2 mRNA production were abolished in spleen cells without anti-CD3 antibody stimulation.
CAPE is an important regulator of CP for cytokine regulation in anti-CD3 antibody-stimulated spleen cells. The agent specifically reduced IFN-γ, IL-6, and IL-17 and slightly enhanced Th2 cytokine production while significantly enhancing IL-2 production at the transcriptional level.
评估中国蜂胶(CP)及其主要成分咖啡酸苯乙酯(CAPE)对抗 CD3 抗体刺激的小鼠脾细胞细胞因子产生的免疫调节作用。
用抗 CD3 单克隆抗体刺激的小鼠脾细胞与 CP、CAPE 和 TRPA1 钙通透性阳离子通道的特异性拮抗剂 HC030031 共培养。通过酶联免疫吸附试验测定细胞因子的产生。通过反转录定量聚合酶链反应检测白细胞介素(IL)-2 mRNA 的表达。
在 1/16000 CP 稀释剂处理的刺激脾细胞中,IL-2 的产生明显增强,而 IL-4 和 IL-10 的产生则没有明显影响。相反,干扰素(IFN)-γ、IL-6 和 IL-17 的产生明显减少。CP 的这些作用可以通过 CAPE 的处理重现。时程观察表明,与对照细胞相比,CAPE 刺激的脾细胞中 IL-2 mRNA 的表达和产生明显增强;然而,与未处理的对照细胞相比,IL-2 的产生明显延迟。HC030031 的加入几乎不能减轻 CAPE 对 IL-2 产生的增强作用。CAPE 对 IL-2 mRNA 产生的这些作用在没有抗 CD3 抗体刺激的脾细胞中被消除。
CAPE 是 CP 调节抗 CD3 抗体刺激的脾细胞细胞因子调节的重要调节剂。该药物特异性降低 IFN-γ、IL-6 和 IL-17,并轻微增强 Th2 细胞因子的产生,同时在转录水平上显著增强 IL-2 的产生。