Rhein inhibits M1 polarization of BV2 microglia through MAPK/IκB signalling pathway and reduces neurotoxicity caused by neuroinflammation

BackgroundRhein is an anthraquinone compound with anti-inflammatory pharmacological activity. It has been found to play a neuroprotective role in neurological diseases, but the neuroprotective mechanism of rhein remains unclear.MethodsSH-SY5Y cells serving as neuron-like cells and BV2 microglia were used. The toxicity of rhein on BV2 microglia and the viability of SH-SY5Y cells were measured by CCK-8 assay. The mRNA expression and secretion of pro-inflammatory cytokines were detected by qPCR and ELISA. Iba1, CD86 and pathway signalling protein in BV2 microglia were assessed by Western blot and immunofluorescence. Apoptosis of SH-SY5Y cells exposed to neuroinflammation was analysed through flow cytometry.ResultsRhein inhibited MAPK/I kappa B signalling pathways. Further studies revealed that rhein inhibited the production of pro-inflammatory cytokines TNF-alpha, IL-6, IL-1 beta and iNOS in BV2 cells and also inhibited the expression of M1 polarization markers Iba1 and CD86 in BV2 cells. Furthermore, rhein reduced the apoptotic rate and restored cell viability of SH-SY5Y cells exposed to neuroinflammation.ConclusionsOur study demonstrated that rhein inhibited microglia M1 polarization via MAPK/I kappa B signalling pathway and protected nerve cells through suppressing neuroinflammation. This study demonstrated that rhein inhibited microglia M1 polarization via MAPK/I kappa B signalling pathway and protected nerve cells through suppressing neuroinflammation. The finding contributed to the understanding of the mechanism by which rhein protected neurons and may promote further research on rhein among CNS diseases. image