Abstract
We set our experiments to investigate the role of GPR84 in LPS-induced acute lung injury. The expression of GPR84 was detected through RT-qPCR and Western blotting (WB) after LPS treatment in ALI mouse and cell model, respectively. Following the treatment of GPR 84 inhibitor, the lung injury was evaluated through HE staining while the MAPK signalling components were analyzed through WB, as well as NF-κB signalling components. These components were further analyzed by the addition of anisomycin or TPA. The analysis of apoptosis was performed through TUNEL staining. We showed that LPS stimulated the expression of GPR84 expression. GPR 84 inhibitor facilitated the activation of MAPK signalling while inhibiting MAPK signalling, these effects of which were further rescued by anisomycin or TPA treatment. In conclusion, our findings support that GPR84 inhibitor improved lung injury caused by LPS and revealed a role of GPR87 modulating NF-κB through MAPK signalling pathway. Altogether, GPR84 could be as a prospective target for the treatment of ALI.
GPR84 inhibitor ameliorated lung inflammation and modulated NF-κB through MAPK signalling pathway