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已发表论文
肠道菌群组成、短链脂肪酸代谢和肠-肾氧化应激之间的相互作用：与腹泻的相关性
Authors Shen J , Fang L, Peng X, Jiang M, Xie X, Tan Z
Received 30 December 2025
Accepted for publication 1 April 2026
Published 20 April 2026 Volume 2026:19 588857
DOI https://doi.org/10.2147/JIR.S588857
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Alberto Caminero
Junxi Shen,1,2 Leyao Fang,1,2 Xinxin Peng,2,3 Miao Jiang,1,2 Xuejiao Xie,1,2 Zhoujin Tan1,2
1School of Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha, Hunan, People’s Republic of China; 2Hunan Key Laboratory of Traditional Chinese Medicine Prescription and Syndromes Translational Medicine, Changsha, Hunan, People’s Republic of China; 3The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, People’s Republic of China
Correspondence: Zhoujin Tan, Email tanzhjin@sohu.com Xuejiao Xie, Email xuejiao123@hnucm.edu.cn
Background: Gut microbiota dysbiosis in the colon, leading to gut-kidney inflammatory responses, is a key cause of exacerbated diarrhea. The upstream mechanistic relationship between colonic microecological disturbance and gut-kidney interaction injury remains unclear.
Methods: In this study, a total of 20 KM mice were used. We established a mouse diarrhea model, analyzed colonic microbiota composition via 16S rRNA sequencing, quantified short-chain fatty acids (SCFAs) using gas chromatography-mass spectrometry (GC-MS), and measured sirtuin 3 (SIRT3), superoxide dismutase 2 (SOD2) protein levels, total SOD activity, and ROS levels in colonic and kidney tissues. Mouse physiological signs and histopathological changes were also evaluated.
Results: In model mice, the relative expression levels of SIRT3 and SOD2 proteins in colon and kidney tissues were significantly decreased (P < 0.01). Similarly, the SOD enzyme activity also showed a significant reduction, with P < 0.05 in the colon and P < 0.01 in the kidney. In contrast, the intensity of ROS was significantly increased (P < 0.01). Colonic microbial diversity declined. Streptococcus showed a significant enrichment in the colon (P < 0.01), and the contents of propionic acid and isobutyric acid were significantly decreased (P < 0.05). A negative correlation was observed between the abundance of Streptococcus and SCFAs, and there were correlations between the abundance of Streptococcus and SOD enzyme activity in tissues as well as ROS intensity.
Conclusion: Therefore, we infer that there are associations between gut microbiota dysbiosis in the colon, altered levels of SCFAs, exacerbated gut-kidney oxidative stress responses, and the onset and progression of diarrhea.
Keywords: gut microbiota, SCFAs, oxidative stress, gut-kidney interaction, diarrhea
1School of Traditional Chinese Medicine, Hunan University of Chinese Medicine, Changsha, Hunan, People’s Republic of China; 2Hunan Key Laboratory of Traditional Chinese Medicine Prescription and Syndromes Translational Medicine, Changsha, Hunan, People’s Republic of China; 3The First Hospital of Hunan University of Chinese Medicine, Changsha, Hunan, People’s Republic of China
Correspondence: Zhoujin Tan, Email tanzhjin@sohu.com Xuejiao Xie, Email xuejiao123@hnucm.edu.cn
Background: Gut microbiota dysbiosis in the colon, leading to gut-kidney inflammatory responses, is a key cause of exacerbated diarrhea. The upstream mechanistic relationship between colonic microecological disturbance and gut-kidney interaction injury remains unclear.
Methods: In this study, a total of 20 KM mice were used. We established a mouse diarrhea model, analyzed colonic microbiota composition via 16S rRNA sequencing, quantified short-chain fatty acids (SCFAs) using gas chromatography-mass spectrometry (GC-MS), and measured sirtuin 3 (SIRT3), superoxide dismutase 2 (SOD2) protein levels, total SOD activity, and ROS levels in colonic and kidney tissues. Mouse physiological signs and histopathological changes were also evaluated.
Results: In model mice, the relative expression levels of SIRT3 and SOD2 proteins in colon and kidney tissues were significantly decreased (P < 0.01). Similarly, the SOD enzyme activity also showed a significant reduction, with P < 0.05 in the colon and P < 0.01 in the kidney. In contrast, the intensity of ROS was significantly increased (P < 0.01). Colonic microbial diversity declined. Streptococcus showed a significant enrichment in the colon (P < 0.01), and the contents of propionic acid and isobutyric acid were significantly decreased (P < 0.05). A negative correlation was observed between the abundance of Streptococcus and SCFAs, and there were correlations between the abundance of Streptococcus and SOD enzyme activity in tissues as well as ROS intensity.
Conclusion: Therefore, we infer that there are associations between gut microbiota dysbiosis in the colon, altered levels of SCFAs, exacerbated gut-kidney oxidative stress responses, and the onset and progression of diarrhea.
Keywords: gut microbiota, SCFAs, oxidative stress, gut-kidney interaction, diarrhea