FC-99 ameliorates sepsis-induced liver dysfunction by modulating monocyte/macrophage differentiation via Let-7a related monocytes apoptosis.

ABSTRACT:

Background

The liver is a vital target for sepsis-related injury, leading to inflammatory pathogenesis, multiple organ dysfunction and high mortality rates. Monocyte-derived macrophage transformations are key events in hepatic inflammation. N¹-[(4-methoxy)methyl]-4-methyl-1,2-benzenediamine (FC-99) previously displayed therapeutic potential on experimental sepsis. However, the underlying mechanism of this protective effect is still not clear.

Results

FC-99 treatment attenuated the liver dysfunction in septic mice that was accompanied with reduced numbers of pro-inflammatory Ly6C^hi monocytes in the peripheral blood and CD11b⁺F4/80^lo monocyte-derived macrophages in the liver. These effects were attributed to the FC-99-induced apoptos

SUBMITTER: Zhao Y 

PROVIDER: S-EPMC5871089 | biostudies-literature | 2018 Mar

REPOSITORIES: biostudies-literature