1 research outputs found
Metformin Protects against LPS-Induced Intestinal Barrier Dysfunction by Activating AMPK Pathway
Metformin not only regulates energy
metabolism but also participates
in many cellular processes. In this study, we investigated the effect
of metformin on lipopolysaccharide (LPS)-induced intestinal barrier
damage. We found that LPS treatment decreased the expression of tight
junction proteins and caused a proinflammatory response and oxidative
stress in the intestine. Interestingly, metformin treatments attenuated
LPS-induced intestinal barrier damage, inflammation, and oxidative
stress. We found that metformin improved the expression of intestinal
tight junction proteins (ZO1, occludin, and Claudin1) that were reduced
by LPS stimulation. Moreover, metformin alleviated LPS-induced NF-κB
phosphorylation, promoted Nrf2 nuclear translocation, and increased
the expression of the antioxidative genes (HO-1 and NQO-1), leading
to reduced intestinal ROS content. Mechanistically, we found that
metformin protects against LPS-induced intestinal barrier dysfunction
by activating AMPK. These results reveal the potential of metformin
as an effective therapy for treating intestinal diseases