ArticleJournal of inflammation research2025
Effects of Emodin on Lung Inflammation and Intestinal Microbes in Chronic Obstructive Pulmonary Disease.
Article in Journal of inflammation research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Introduction: The impact of COPD on human health is enormous. Emodin, which has anti-inflammatory, anti-cancer, spasmolysis, and laxative effects, has not been systematically investigated within a study with regard to the treatment of COPD. Methods: In this study, we conducted Experiment 1 to evaluate the effects of emodin on COPD. Emodin was purchased from Shanghai Yuanye Biotechnology Co. Ltd. (batch number: T17A10F95418). Pathological changes in lung tissue and the average lung lining interval were used to evaluate the severity of emphysema. Inflammatory cell counts in alveolar lavage fluid and the ratio of neutrophils and lymphocytes were used to observe the level of inflammation. The level of HMGB1-RAGE expression was determined via PCR. Moreover, we compared changes in the metabolites of the intestinal microbial community following an intervention with emodin. In Experiment 2, we observed the effect of fecal on the inflammatory response in COPD mice. A mouse dual intervention model was established using flora depletion and COPD modeling. We evaluated the general health of the model mice, specific pathological changes in lung tissue, the average lung lining interval, inflammatory cell counts within the alveolar lavage fluid, and HMGB1-RAGE pathway expression. Results: Our results demonstrated that emodin statistically significantly improved lung tissue inflammation in COPD mice, and that butanoic acid was the main differential metabolite in intestinal bacteria. Transplanting the feces of the emodin group mice in Experiment 1 to the model mice evaluated in Experiment 2 reduced the infiltration of inflammatory cells and down-regulated the HMGB1-RAGE inflammation pathway. Conclusion: Our findings provide important information for guiding future research directions.
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