Effects of quercetin on Aβ25-35-mediated mitochondrial apoptosis pathway and p38MAPK signal pathway
OBJECTIVE To investigate the effect of quercetin(Que)on mitochondrial damage induced by Aβ25-35 through p38MAPK signaling pathway in PC12 cells.METHODS PC12 cells were treated with Aβ25.35(20 μmol·L-1)as a model of AD cell toxicity,and 0.1 μmol·L-1 of 17β-estradiol(17β-E2)and 50 μmol·L-1 of genistein(Gen)served as positive controls,low-dose Que(40 μmol·L-1),medium-dose Que(60 μmol·L-1)and high-dose Que(80 μmol·L-1)were used in this experiment.And select the SB203580(p38MAPK specific inhibitor)as pretreatment group(Aβ25-35+10 μmol·L-1 SB203580).Mito-Tracker-red detects Mitochondria morphology;JC-1 detects mitochondrial membrane potential and luciferase luminescence detects ATP;Immunofluorescence staining detects the expression of p-p38MAPK protein.Western blot method determines the expression of Bcl-2,Bax,p-p38MAPK/p38MAPK and Cytochrome C(Cyt C)protein.RESULTS Compared with the model group,quercetin significantly increased mitochondrial membrane potential and ATP content,and protected mitochondrial morphol-ogy.Quercetin significantly inhibited the phosphorylation of p38MAPK.Western blot showed'that quercetin up-regulated the expression of Bcl-2 protein and down-regulated the expression of Bax,p-p38MAPK/p38MAPK and Cyt C protein(P＜0.05).When p38MAPK was inhibited by SB203580,compared with the model group,the expression of Bax and Cyt C protein decreased(P＜0.01),while the expression of Bcl-2 protein increased(P＜0.01).CONCLUSION Quercetin can inhibit A by mediating the p38MAPK signaling pathway β mitochondrial apoptosis induced by 25-35 exerts neuroprotective effects.
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