The impact of burdock tea (BT) made from burdock (Arctium lappa) roots in normal individuals and animal models remains largely unknown, particularly on lung protection. This study examined responses of oxidative stress, inflammation, and the microbiota within the cecum and the lung to BT treatment in healthy Wistar rats. A middle-dose BT reduced the Chao1 and Shannon indices, and both low and middle doses induced structural alterations in the cecal microbiota. Additionally, low doses increased the abundances of Phascolarctobacterium, Alloprevotella, Desulfovibrio, and the NK4A214 group. In the lung, middle and high doses increased Corynebacterium, with high doses also boosting Megasphaera and Lactobacillus. Functionally, low doses downregulated the biosynthesis of antibiotics in the cecal microbiota, while middle doses reduced the Epstein–Barr virus and Escherichia coli pathogenic infection pathways; additionally, middle and high doses modulated chromosomal proteins and bile acid biosynthesis in the pulmonary microbiota. BT treatment enhanced the content of short-chain fatty acids (SCFAs), upregulated the expression of GPR43, and suppressed NLRP3 expression in both the colon and lung tissues, while concurrently promoting the expression of ZO-1 and Occludin. Furthermore, serum levels of IL-1β and IL-6, as well as tissue levels of MDA, were significantly reduced. Notably, propionate exhibited an inverse correlation with MDA, IL-6, and NLRP3, while showing a positive correlation with ZO-1. Similarly, acetate was negatively correlated with MDA and NLRP3 and positively correlated with ZO-1. Overall, BT exhibits a nontoxic profile and may protect lung tissue through its antioxidant nature and gut–lung axis mediated by SCFAs.

The impacts of Burdock tea (BT) made from Burdock (Arctium lappa) roots on normal individuals and animal models is largely unknown, particularly on lung protection. This study examined responses of oxidative stress, inflammation, and the microbiota within the cecum and lung to BT treatment in healthy Wistar rats. A middle-dose BT reduced the Chao1 and Shannon indices, and both low and middle doses induced structural alterations in the cecal microbiota. Low dose increased Phascolarctobacterium, Alloprevotella, Desulfovibrio, and the NK4A214 group. In the lung, middle and high doses raised Corynebacterium, with high dose also boosting Megasphaera and Lactobacillus. Functionally, low dose downregulated antibiotics biosynthesis in the cecal microbiota, while middle dose reduced Epstein-Barr virus and Escherichia coli pathogenic infection pathways; additionally, middle and high doses modulated chromosomal proteins and bile acid biosynthesis in the pulmonary microbiota. BT increased short-chain fatty acids content, upregulated GPR43, and reduced NLRP3 expression in both colon and lung while enhancing ZO-1 and occludin. Serum IL-1β and IL-6 and tissue MDA levels also decreased, with propionate inversely correlated with MDA, IL-6, NLRP3 and positively with ZO-1. Overall, BT exhibits a nontoxic profile and may protect lung tissue through its antioxidant nature and gut-lung axis mediated by SCFAs.