ObjectiveTo explore the role of miR-34c in regulating NLRP3 inflammasome to activate the caspase-1 signaling pathway to induce microglia pyrolysis.

MethodsAfter the observation of lipopolysaccharide (LPS) combined with ATP for activating microglia, the release of lactate dehydrogenase (LDH) was detected using LDH cytotoxicity detection kit to determine the integrity of the microglia cell membrane; then, the microglia transfected with miR-34c are activated by LPS and ATP, which was observed for the changes in glial cell membrane; cell proliferation and toxicity detection kit (CCK-8) was used to detect changes in the viability of miR-34c transfected microglia and untransfected microglia under the stimulation of LPS and ATP; Western blotting was used to detect the protein expression in LPS+ATP-induced microglia and microglia after miR-34c transfection, such as NLRP3 inflammasome, caspase-1, GSDMD, IL-1β, IL-18.

ResultsCompared with normal microglia, the expression of miR-34c in microglia induced by LPS+ATP combination decreased (P < 0.01);the LDH release level of microglia in the observation group was lower than that in the control group (P < 0.01);in the CCK-8 cell viability test, there was no significant difference of the microglia viability between the two groups on the first day(P>0.05), while the observation group was significantly higher than the control group at other times (P < 0.01);the production of NLRP3 inflammasome, caspase-1, GSDMD, IL-1β and IL-18 of microglia in the observation group was decreased compared with those in the control group (P < 0.01).

ConclusionsMiR-34c can inhibit LPS+ATP-induced microglial pyroptosis, which may be related to the reduction of NLRP3 inflammasome activation and key proteins expression in the downstream caspase-1-dependent pyroptosis signaling pathway.