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已发表论文
扶正解毒方通过调节肠道微生物群增强短链脂肪酸改善急性肺损伤
Authors Chen J, Pan S, Huo W, Wang W, Tan Z, Wu Y, Kong Y, Yin C, Gan K, Zhao M, Gao M, Xia Q, Li J, Lu Y, Yang R, Liu Y
Received 28 July 2025
Accepted for publication 25 December 2025
Published 10 February 2026 Volume 2026:19 556752
DOI https://doi.org/10.2147/JIR.S556752
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Tara Strutt
Jiankun Chen,1,2,* Simin Pan,2,* Wanhua Huo,2 Weiye Wang,2 Zhaoqi Tan,2 Yuan Wu,1 Yunqi Kong,2 Chubo Yin,2 Kao Gan,2,3 Meng Zhao,4 Ming Gao,2,5 Qinghua Xia,6 Jiqiang Li,1 Yue Lu,7 Rongyuan Yang,8,9 Yuntao Liu3,8,9
1Department of The Third General, The Second Affiliated Hospital Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, People’s Republic of China; 2The Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, People’s Republic of China; 3Department of Emergency, The Second Affiliated Hospital Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, People’s Republic of China; 4School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, People’s Republic of China; 5Department of Emergency, Nanhai District Hospital of Chinese Medicine (Guangdong Provincial Hospital of Integrated Chinese and Western Medicine), Foshan, People’s Republic of China; 6Department of Respiratory, Qingyuan Hospital of Chinese Medicine, Qingyuan, People’s Republic of China; 7Research Team of Bio-Molecular and System Biology of Chinese Medicine, Guangdong Academy of Traditional Chinese Medicine, Guangzhou, Guangdong Province, People’s Republic of China; 8State Key Laboratory of Traditional Chinese Medicine Syndrome, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, People’s Republic of China; 9Guangdong Provincial Key Laboratory of Research on Emergency in TCM, Guangzhou, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Rongyuan Yang, Email yrr126@126.com Yuntao Liu, Email iamliuyuntao@163.com
Aim of Study: The objective of this research is to clarify the mechanism by which FZJDF mitigates lipopolysaccharide (LPS)- ALI through the enhancement of short-chain fatty acids (SCFAs) production by Clostridium butyricum (C. butyricum), and the modulation of the gut microbiota-gut-lung axis.
Materials and Methods: The mice were treated with FZJDF for 7 days and then treated with LPS. The therapeutic efficacy of FZJDF against LPS-induced ALI was evaluated through lung-to-weight ratio, Inflammatory factor, pathological changes. Additionally, the intestinal barrier function was evaluated by analyzing tight junction protein expression levels. 16S rRNA gene sequencing was employed to monitor alterations in the intestinal microbiome and pulmonary microbiota, while gas chromatography-mass spectrometry (GC-MS) and ultra-performance liquid chromatography (UPLC) were utilized to quantify the concentrations of SCFAs. Ultimately, the necessity of C. butyricum for FZJDF’s therapeutic influence was confirmed through antibiotic-mediated gut microbiota depletion.
Results: FZJDF significantly decreased lung-to-weight ratio and reducing inflammatory cell infiltration of neutrophils. Furthermore, it significantly elevated the expression levels of tight junction proteins. It is plausible that FZJDF may improve intestinal and lung microecological imbalance and stimulate the synthesis of SCFAs. Notably, we determine C. butyricum as the crucial bacterium for the role of FZJDF in gut barrier repair and suppression of lung inflammation in ALI mice. The use of antibiotics led to the repair of the intestinal barrier and a failure in SCFAs production, whereas C. butyricum colonization restores the therapeutic effect of FZJDF in ALI mice, further confirming that FZJDF attenuates ALI.
Conclusion: Our results imply that FZJDF could exert its palliative effect in ALI by regulating the intestinal microbiota to increase the production of SCFAs, which in turn inhibits neutrophil-mediated inflammatory responses. These findings support microbiota-targeted traditional medicine as a translational strategy for acute lung injury.
Keywords: fuzhengjiedu formula, LPS-induced ALI, short-chain fatty acids, gut-lung axis
1Department of The Third General, The Second Affiliated Hospital Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, People’s Republic of China; 2The Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, People’s Republic of China; 3Department of Emergency, The Second Affiliated Hospital Guangzhou University of Chinese Medicine (Guangdong Provincial Hospital of Chinese Medicine), Guangzhou, People’s Republic of China; 4School of Pharmaceutical Sciences, Guangzhou University of Chinese Medicine, Guangzhou, People’s Republic of China; 5Department of Emergency, Nanhai District Hospital of Chinese Medicine (Guangdong Provincial Hospital of Integrated Chinese and Western Medicine), Foshan, People’s Republic of China; 6Department of Respiratory, Qingyuan Hospital of Chinese Medicine, Qingyuan, People’s Republic of China; 7Research Team of Bio-Molecular and System Biology of Chinese Medicine, Guangdong Academy of Traditional Chinese Medicine, Guangzhou, Guangdong Province, People’s Republic of China; 8State Key Laboratory of Traditional Chinese Medicine Syndrome, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, People’s Republic of China; 9Guangdong Provincial Key Laboratory of Research on Emergency in TCM, Guangzhou, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Rongyuan Yang, Email yrr126@126.com Yuntao Liu, Email iamliuyuntao@163.com
Aim of Study: The objective of this research is to clarify the mechanism by which FZJDF mitigates lipopolysaccharide (LPS)- ALI through the enhancement of short-chain fatty acids (SCFAs) production by Clostridium butyricum (C. butyricum), and the modulation of the gut microbiota-gut-lung axis.
Materials and Methods: The mice were treated with FZJDF for 7 days and then treated with LPS. The therapeutic efficacy of FZJDF against LPS-induced ALI was evaluated through lung-to-weight ratio, Inflammatory factor, pathological changes. Additionally, the intestinal barrier function was evaluated by analyzing tight junction protein expression levels. 16S rRNA gene sequencing was employed to monitor alterations in the intestinal microbiome and pulmonary microbiota, while gas chromatography-mass spectrometry (GC-MS) and ultra-performance liquid chromatography (UPLC) were utilized to quantify the concentrations of SCFAs. Ultimately, the necessity of C. butyricum for FZJDF’s therapeutic influence was confirmed through antibiotic-mediated gut microbiota depletion.
Results: FZJDF significantly decreased lung-to-weight ratio and reducing inflammatory cell infiltration of neutrophils. Furthermore, it significantly elevated the expression levels of tight junction proteins. It is plausible that FZJDF may improve intestinal and lung microecological imbalance and stimulate the synthesis of SCFAs. Notably, we determine C. butyricum as the crucial bacterium for the role of FZJDF in gut barrier repair and suppression of lung inflammation in ALI mice. The use of antibiotics led to the repair of the intestinal barrier and a failure in SCFAs production, whereas C. butyricum colonization restores the therapeutic effect of FZJDF in ALI mice, further confirming that FZJDF attenuates ALI.
Conclusion: Our results imply that FZJDF could exert its palliative effect in ALI by regulating the intestinal microbiota to increase the production of SCFAs, which in turn inhibits neutrophil-mediated inflammatory responses. These findings support microbiota-targeted traditional medicine as a translational strategy for acute lung injury.
Keywords: fuzhengjiedu formula, LPS-induced ALI, short-chain fatty acids, gut-lung axis