Department of Food Science and Technology, Seoul National University of Science and Technology, Seoul 01811, Republic of Korea.
Department of Nano Bio Engineering, Seoul National University of Science and Technology, Seoul 01811, Republic of Korea.
J Microbiol Biotechnol. 2023 Apr 28;33(4):493-499. doi: 10.4014/jmb.2212.12041. Epub 2023 Jan 20.
In this study we evaluated the immune-enhancing effects of β-glucan, the main component of (), and on inflammatory factor expression in RAW264.7 macrophages and ICR mice with cyclophosphamide-induced immunosuppression. Macrophages were treated with β-glucan or for 48 h. The β-glucan and groups exhibited higher levels of inducible nitric oxide synthase, nitric oxide, and tumor necrosis factor (TNF)-α than the control (vehicle alone) group. Animals were fed saline and β-glucan (400 mg/kg body weight (B.W.)) or (400 or 800 mg/kg B.W.) for 19 days, and on days 17-19, cyclophosphamide (CCP, 80 mg/kg B.W.) was administered to induce immunosuppression in the ICR mouse model. CCP reduced the body weight, spleen index, and cytokine expression of the mice. To measure cytokine and receptor expression, splenocytes were treated with concanavalin A (ConA) or lipopolysaccharide (LPS) as a mitogen for 24 h. In vivo, ConA stimulation significantly upregulated the expression of interferon (IFN)-γ, interleukin (IL)-10, IL-12 receptor β1, IL-1β, and IL-2 in splenocytes from the β-glucan- or -treated groups compared with those in the splenocytes from the CCP-treated group; LPS stimulation increased the levels of the cytokines TNF-α, IL-1β, and IL-6 in splenocytes from the β-glucan- or -treated groups compared with those from the CCP-treated group, but most of these differences were not significant. These results demonstrate the effect of in ameliorating macrophages and immunosuppression in CCP-treated mice. Thus, has the potential to enhance macrophage- and splenocyte-mediated immune-stimulating responses.
在这项研究中，我们评估了 β-葡聚糖（）和（）的主要成分对环磷酰胺诱导免疫抑制的 RAW264.7 巨噬细胞和 ICR 小鼠炎症因子表达的免疫增强作用。巨噬细胞用 β-葡聚糖或处理 48 小时。与对照组（单独给予载体）相比，β-葡聚糖和组诱导型一氧化氮合酶、一氧化氮和肿瘤坏死因子（TNF）-α的水平更高。动物给予生理盐水和β-葡聚糖（400mg/kg 体重（B.W.））或（400 或 800mg/kg B.W.）19 天，在第 17-19 天，给予环磷酰胺（CCP，80mg/kg B.W.）诱导 ICR 小鼠模型免疫抑制。CCP 降低了小鼠的体重、脾脏指数和细胞因子表达。为了测量细胞因子和受体表达，用刀豆蛋白 A（ConA）或脂多糖（LPS）作为有丝分裂原处理脾细胞 24 小时。在体内，与 CCP 处理组的脾细胞相比，ConA 刺激显著上调了β-葡聚糖或处理组的脾细胞中干扰素（IFN）-γ、白细胞介素（IL）-10、IL-12 受体 β1、IL-1β 和 IL-2 的表达；LPS 刺激增加了β-葡聚糖或处理组的脾细胞中细胞因子 TNF-α、IL-1β 和 IL-6 的水平，但这些差异大多数并不显著。这些结果表明在改善 CCP 处理的小鼠的巨噬细胞和免疫抑制方面的作用。因此，具有增强巨噬细胞和脾细胞介导的免疫刺激反应的潜力。
