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黑灵芝多糖对 LPS 诱导的炎症巨噬细胞模型和肠道样 Caco-2/巨噬细胞共培养炎症模型的调控作用。

Regulatory effects of Ganoderma atrum polysaccharides on LPS-induced inflammatory macrophages model and intestinal-like Caco-2/macrophages co-culture inflammation model.

机构信息

State Key Laboratory of Food Science and Technology, China-Canada Joint Lab of Food Science and Technology (Nanchang), Nanchang University, 235 Nanjing East Road, Nanchang, 330047, China.

State Key Laboratory of Food Science and Technology, China-Canada Joint Lab of Food Science and Technology (Nanchang), Nanchang University, 235 Nanjing East Road, Nanchang, 330047, China.

出版信息

Food Chem Toxicol. 2020 Jun;140:111321. doi: 10.1016/j.fct.2020.111321. Epub 2020 Apr 11.

Abstract

Lipopolysaccharide (LPS)-induced inflammatory macrophages model and intestinal-like Caco-2/macrophages co-culture inflammation model were established to evaluate the anti-inflammatory effect and underlying mechanism of Ganoderma atrum polysaccharides (PSG-1). It was found that PSG-1 reduced LPS-induced secretion of pro-inflammatory cytokine (TNF-α, IL-6 and IL-1β), ROS levels, and inhibited the expression of COX-2 in LPS-stimulated inflammatory macrophages model and intestinal-like Caco-2/macrophages co-culture inflammation model. Furthermore, PSG-1 suppressed the LPS-induced activation of MAPKs signaling pathways, and regulated oxidative stress by activating the Nrf2/Keap1 signaling pathways. These above results indicated that PSG-1 not only has a direct anti-inflammatory effect in LPS-induced inflammatory macrophages model, but also has an indirect anti-inflammatory effect in intestinal-like Caco-2/macrophages co-culture inflammation model. These findings provide new insight of the mechanism underlying the anti-inflammatory activities of PSG-1, and facilitated the expansion of the application of PSG-1 in natural functional food.

摘要

脂多糖 (LPS)-诱导的炎症巨噬细胞模型和肠样 Caco-2/巨噬细胞共培养炎症模型被建立来评估灵芝多糖 (PSG-1) 的抗炎作用和潜在机制。研究发现 PSG-1 降低了 LPS 诱导的促炎细胞因子 (TNF-α、IL-6 和 IL-1β) 的分泌、ROS 水平,并抑制了 LPS 刺激的炎症巨噬细胞模型和肠样 Caco-2/巨噬细胞共培养炎症模型中 COX-2 的表达。此外,PSG-1 通过激活 Nrf2/Keap1 信号通路抑制 LPS 诱导的 MAPKs 信号通路的激活,从而调节氧化应激。这些结果表明 PSG-1 不仅在 LPS 诱导的炎症巨噬细胞模型中具有直接的抗炎作用,而且在肠样 Caco-2/巨噬细胞共培养炎症模型中具有间接的抗炎作用。这些发现为 PSG-1 的抗炎活性的潜在机制提供了新的见解,并促进了 PSG-1 在天然功能性食品中的应用扩展。

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