Magnesium-based materials are promising
biodegradable implants, although the impact of
magnesium on rectal anastomotic
inflammation is poorly understood. Thus, we investigated the inflammatory effects of high-purity Mg staples in rectal anastomoses by in vivo
luciferase reporter gene expression in transgenic mice,
hematoxylin-
eosin staining, immunohistochemistry, and Western blotting. As expected, strong IL-1β-mediated
inflammation and inflammatory cell infiltration were observed 1 day after rectal anastomoses were stapled with high-purity Mg or Ti. However,
inflammation and inflammatory cell infiltration decreased more robustly 4-7 days postoperation in tissues stapled with high-purity Mg. This rapid reduction in
inflammation was confirmed by immunohistochemical analysis of
IL-6 and TNF-α. Western blot also suggested that the reduced inflammatory response is due to suppressed TLR4/NF-κB signaling. In contrast, MCP-1, uPAR, and
VEGF were abundantly expressed, in line with the notion that expression of these
proteins is regulated by feedback between the
VEGF and NF-κB pathways. In vitro expression of MCP-1, uPAR, and
VEGF was also similarly high in primary rectal mucosal epithelial cells exposed to extracts from Mg staples, as measured by antibody array. Collectively, the results suggest that high-purity Mg staples suppress the inflammatory response during rectal anastomoses via TLR4/NF-κB and
VEGF signaling.