Atractylenolide III inhibits epithelial­mesenchymal transition in small intestine epithelial cells by activating the AMPK signaling pathway.

ABSTRACT

Compared with the available drugs for the treatment of fibrosis in other organs, the development of intestinal anti­fibrosis drugs is limited. Therefore, it is of practical significance to examine novel drugs to delay or block the development of intestinal fibrosis. The present study aimed to investigate the effect of atractylenolide III (ATL­III) on intestinal fibrosis. An MTT assay was used to detect the effect of ATL­III on the activity of IEC­6 cells. The migration and invasion of fibrotic cells stimulated with TGF­ß were determined via wound healing and Transwell assays. An immunofluorescence assay and western blotting were conducted to assess the expression levels of protein associated with epithelial­mesenchymal transition (EMT). The role of the AMP­activated protein kinase (AMPK) pathway was verified using compound C (an AMPK inhibitor) treatment. The results of the present study indicated that ATL­III had no effect on the cells at a dose of 1­20 µmol/l. Moreover, ATL­III can inhibit the invasion and migration of cells induced by TGF­ß1, as well as block the EMT process. It was found that ATL­III could also activate the AMPK pathway. Furthermore, compound C reduced the inhibitory effect of ATL­III on stimulated cells, which indicated that the AMPK pathway plays a role in the inhibition process. In conclusion, ATL­III may inhibit the EMT of IEC­6 cells stimulated with TGF­ß1 by activating the AMPK signaling pathway.