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Burdock Tea Affects Pulmonary Microbiota and Physiology Through Short-Chain Fatty Acids in Wistar Rats
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Burdock Tea Affects Pulmonary Microbiota and Physiology Through Short-Chain Fatty Acids in Wistar Rats
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Journal Article
Burdock Tea Affects Pulmonary Microbiota and Physiology Through Short-Chain Fatty Acids in Wistar Rats
2025
Overview
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.
