Mechanism And Pharmacological Studies Of Parkinson's Disease Based On The Effects Of Caspase11

Objective:To investigate the effects of polygalasaponin F(PS-F)on LPS-induced inflammasome Caspase11 activation in BV2 cells and explore the potential anti-inflammatory mechanism of PS-F.Methods:The experiment divided into 5 groups,including the control group,the model group and PS-F treatment groups(0.10,1.00,10.00 ?mol·L-1).ELISA,Quantitative real-time PCR and Western blot were used to assay the mRNA and protein expression of IL-1?.The levels of NLRP3,caspasel,ASC,caspasell protein were examined by the Western blot analysis.The experiment divided into 3 groups,including the control group,the model group and SP600125 treatment groups.Immunofluorescence,Quantitative real-time PCR and Western blot were used to assay the mRNA and protein expression of Caspasell.The levels of Caspase11?LC3?P62?PJNK protein were examined by the Western blot analysis.Results:Compared with the model group,the PS-F treatment groups effectively reduced the IL-1? expression in LPS-induced inflammatory model in a dose-dependent manner(p<0.01 or p<0.05).Morover,PS-F significantly inhibited the ASC and caspasell expression(p<0.01).Compared with the model group,the SP600125 treatment groups effectively reduced the Caspasell expression in LPS-induced inflammatory model in a dose-dependent manner(p<0.01 orp<0.05).Morover,SP600125 significantly inhibited the P62 and PJNK expression.Conclusions PS-F inhibited the expression of inflammatory mediator IL-1? by suppressing the activation of NLRP3 inflammasome and inhibiting caspasell in LPS-stimulated BV2 cells.SP600125 inhibited the expression of Caspasell by suppressing the activation of JNK signaling and autophagy in LPS-stimulated BV2 cells.