Neutral Polysaccharide from Platycodonis Radix-Ameliorated PM2.5-Induced Lung Injury by Inhibiting the TLR4/NF-κB p65 Pathway and Regulating the Lung and Gut MicrobiomeClick to copy article linkArticle link copied!
- Yang SunYang SunCollege of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, ChinaMore by Yang Sun
- Yanchun WangYanchun WangCollege of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, ChinaMore by Yanchun Wang
- Zaiming YangZaiming YangCollege of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, ChinaMore by Zaiming Yang
- Xianlei HanXianlei HanCollege of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, ChinaMore by Xianlei Han
- Yue ZhangYue ZhangCollege of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, ChinaMore by Yue Zhang
- Liyan ChenLiyan ChenInstitute of Chinese Materia Medica, Heilongjiang Academy of Chinese Medicine Sciences, Harbin 150036, ChinaMore by Liyan Chen
- Jinhai HuoJinhai HuoInstitute of Chinese Materia Medica, Heilongjiang Academy of Chinese Medicine Sciences, Harbin 150036, ChinaMore by Jinhai Huo
- Rina WuRina WuCollege of Food Science, Shenyang Agricultural University, Shenyang 110866, PR ChinaMore by Rina Wu
- Weiming Wang*Weiming Wang*Email: [email protected]Institute of Chinese Materia Medica, Heilongjiang Academy of Chinese Medicine Sciences, Harbin 150036, ChinaMore by Weiming Wang
- Nan Wang*Nan Wang*Email: [email protected]College of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, ChinaMore by Nan Wang
Abstract

Platycodonis radix (PR) has been reported to play a protective role in lung injury. However, much less is known about the protective effect and mechanism of its main component PR polysaccharides (PRPs) in particulate matter (PM2.5)-induced lung injury. Here, a neutral polysaccharide (MW: 244.56 kDa) was isolated from PR, mainly composed of Rha, Ara, Gal, Glc, Xyl, and Man. PRPs significantly improved PM2.5-induced pulmonary edema, oxidative damage, and cell apoptosis and downregulated inflammatory factor levels in bronchoalveolar lavage fluid. Mechanistically, PRPs reduced intestinal mucosal barrier damage, thereby lowering serum lipopolysaccharide levels and inhibiting the overactivation of the TLR4/NF-κB signaling pathway in the lung tissue. Notably, PRPs could optimize the composition of pulmonary and intestinal microbiota. Oral administration of PRPs resulted in enrichment of short-chain fatty acid (SCFA)-producing bacteria, thereby upregulating the levels of acetate, butyrate, and isovalerate. Taken together, PRPs have great potential in preventing and repairing the lung injury caused by PM2.5.
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