Supplementation of Clostridium butyricum Alleviates Vascular Inflammation in Diabetic Mice

• Published in: Diabetes & metabolism journal Vol. 48; no. 3; pp. 390 - 404
• Main Authors: Tian Zhou, Shuo Qiu, Liang Zhang, Yangni Li, Jing Zhang, Donghua Shen, Ping Zhao, Lijun Yuan, Lianbi Zhao, Yunyou Duan, Changyang Xing
• Format: Journal Article
• Language: Korean
• Published: 대한당뇨병학회 2024
• Subjects: Clostridium butyricum; Diabetes mellitus; Gastrointestinal microbiome; NF-E2-related factor 2; Vascular diseases
• ISSN: 2233-6079; 2233-6087

Background: Gut microbiota is closely related to the occurrence and development of diabetes and affects the prognosis of diabetic complications, and the underlying mechanisms are only partially understood. We aimed to explore the possible link between the gut microbiota and vascular inflammation of diabetic mice. Methods: The db/db diabetic and wild-type (WT) mice were used in this study. We profiled gut microbiota and examined the and vascular function in both db/db group and WT group. Gut microbiota was analyzed by 16s rRNA sequencing. Vascular function was examined by ultrasonographic hemodynamics and histological staining. Clostridium butyricum (CB) was orally administered to diabetic mice by intragastric gavage every 2 days for 2 consecutive months. Reactive oxygen species (ROS) and expression of nuclear factor erythroid-derived 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were detected by fluorescence microscopy. The mRNA expression of inflammatory cytokines was tested by quantitative polymerase chain reaction. Results: Compared with WT mice, CB abundance was significantly decreased in the gut of db/db mice, together with compromised vascular function and activated inflammation in the arterial tissue. Meanwhile, ROS in the vascular tissue of db/db mice was also significantly increased. Oral administration of CB restored the protective microbiota, and protected the vascular function in the db/db mice via activating the Nrf2/HO-1 pathway. Conclusion: This study identified the potential link between decreased CB abundance in gut microbiota and vascular inflammation in diabetes. Therapeutic delivery of CB by gut transplantation alleviates the vascular lesions of diabetes mellitus by activating the Nrf2/HO-1 pathway.