You Ye-Lim, Byun Ha-Jun, Chang Yeok Boo, Kim Hyeongyeong, Lee Hyowon, Suh Hyung Joo, Jeon Jin-Young, Kim Bo-Ra, Hwang Ji Eun, Lee Jun Hee, Choi Hyeon-Son
Department of Food Nutrition, Sangmyung University, Seoul 03016, Republic of Korea.
Department of Integrated Biomedical and Life Science, Graduate School, Korea University, Seoul 02841, Republic of Korea.
Int J Biol Macromol. 2025 Mar;296:139671. doi: 10.1016/j.ijbiomac.2025.139671. Epub 2025 Jan 9.
This study aimed to investigate the effects of β-glucan derived from Euglena gracilis (EGB), an edible microalga, on particulate matter (PM)-induced airway inflammation in A549 cells and BALB/c mice. EGB effectively suppressed the mRNA and protein levels of inflammatory cytokines (IL-6, IL-1β, TNF-α, IL-8) and mediators (iNOS, COX-2), while inhibiting the NF-κB and MAPK signaling pathways triggered by PM exposure and reducing nuclear NF-κB levels. Additionally, EGB decreased PM-induced ROS production and increased the protein levels of NRF2 and HO-1, along with genes encoding antioxidant enzymes (catalase, GPx, SOD1), associated with elevated nuclear NRF2 levels. EGB reduced immune cell infiltration and inflammatory cytokine levels in BALF and serum, both of which increased by PM exposure. EGB also significantly increased alveolar numbers while decreasing the gene expression of MMP1/9/13. Furthermore, EGB suppressed PM-induced bronchial thickening and collagen-1 deposition by downregulating TGF-β1 expression, and alleviated goblet cell hyperplasia and mucin production in lung tissues. These results suggest that EGB effectively reduces PM-induced airway inflammation by suppressing NF-κB and MAPK signaling pathways, lowering pro-inflammatory cytokines, and activating the NRF2-HO-1 signaling pathway to enhance antioxidant enzyme expression. This study highlights the potential of EGB as an edible functional agent for controlling PM-related airway inflammation.
本研究旨在探讨源自可食用微藻纤细裸藻的β-葡聚糖(EGB)对颗粒物(PM)诱导的A549细胞和BALB/c小鼠气道炎症的影响。EGB有效抑制炎性细胞因子(IL-6、IL-1β、TNF-α、IL-8)和介质(iNOS、COX-2)的mRNA和蛋白水平,同时抑制PM暴露触发的NF-κB和MAPK信号通路并降低核NF-κB水平。此外,EGB减少PM诱导的ROS产生并增加NRF2和HO-1的蛋白水平,以及与核NRF2水平升高相关的抗氧化酶(过氧化氢酶、谷胱甘肽过氧化物酶、超氧化物歧化酶1)编码基因。EGB减少了BALF和血清中的免疫细胞浸润及炎性细胞因子水平,二者均因PM暴露而升高。EGB还显著增加肺泡数量,同时降低MMP1/9/13的基因表达。此外,EGB通过下调TGF-β1表达抑制PM诱导的支气管增厚和胶原蛋白-1沉积,并减轻肺组织中的杯状细胞增生和粘蛋白产生。这些结果表明,EGB通过抑制NF-κB和MAPK信号通路、降低促炎细胞因子并激活NRF2-HO-1信号通路以增强抗氧化酶表达,有效减轻PM诱导的气道炎症。本研究突出了EGB作为控制PM相关气道炎症的可食用功能剂的潜力。