Abstract
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 <i>db/db</i> diabetic and wild-type (WT) mice were used in this study. We profiled gut microbiota and examined the and vascular function in both <i>db/db</i> 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 <i>db/db</i> mice, together with compromised vascular function and activated inflammation in the arterial tissue. Meanwhile, ROS in the vascular tissue of <i>db/db</i> mice was also significantly increased. Oral administration of CB restored the protective microbiota, and protected the vascular function in the <i>db/db</i> 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.
Funder
National Natural Science Foundation of China
Innovative Talent Promotion Program of Shaanxi Province
Aerospace Medical Research
Publisher
Korean Diabetes Association
Cited by
1 articles.
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