Cordycepin induces M1/M2 macrophage polarization to attenuate the liver and lung damage and immunodeficiency in immature mice with sepsis via NF-κB/p65 inhibition.

Abstract

To explore the impacts of cordycepin and underlying mechanism on the sepsis. The sepsis mice model was built and treated with different concentrations of cordycepin. Then the liver and lung injury caused by cecal ligation and puncture (CLP) was assessed using H&E staining and TUNEL assay. The expression of relevant genes was detected using qRT-PCR analysis and ELISA assays. Besides, the macrophage polarization was checked by flow cytometry. Cordycepin could significantly improve the liver and lung injury. Moreover, cordycepin increased the distribution of F4/80+ CD206+ M2-like macrophages and F4/80+ iNOS+ M1-like macrophages through down-regulating the expression of relevant genes. More importantly, cordycepin could monitor the protein expression of iNOS, Arg-1, TNF-α, MCP-1, IL-4 and IL-10 in CLP mice. Meanwhile, the elevated level of p65 induced by CLP was also repressed by the increase of the cordycepin. Moreover, cordycepin played a crucial part in CLP mice through modulating the NF-κB/p65 signalling pathway. Cordycepin played an important role in mice with sepsis via reducing the M1/M2 macrophage polarization and modulating the NF-κB/p65 signalling pathway.