Effects of tricholoma matsutake polysaccharides on 1-methy-4-pehnyl-pyridine ion-induced PC12 cell damage
Objective To investigate the protective mechanism of tricholoma matsutake polysaccharides(TMP)against 1-methy-4-pehnyl-pyridine ion(MPP+)-induced PC12 cell damage.Methods An Parkinson's disease(PD)PC12 cell model in vitro was constructed using MPP+,and PC12 cell were randomly divided into 5 groups:control group(Ctrl),model group(MDL),TMP high concentration(250 μg/L)group(TMP-H),TMP medium concentration(50 μg/L)group(TMP-M),and TMP low concentration(10 μg/L)group(TMP-L),3 complex wells in each group.Matsutake polysaccharide treated PC12 cells for 24 hours,250 μmol/L MPP+induced PC12 cells were prepared for 24 hours to prepare PD cell models.The cell viability of each group of PC12 cell was detected by CCK-8 method,the lactate dehydrogenase(LDH)release of each group of PC12 cell was detected by LDH method,mitochondrial activity was detected by fluorescence microscopy,the average length of mitochondrial network branches and the number of network branches were calculated by Image J 1.53 r software,the mitochondrial membrane potential was detected by JC-1 method,and the protein Bcl-2/Bax ratio was detected by Western blotting method.Results Compared with the Ctrl group,the survival rate of PC12 cell in the MDL group decreased,the LDH release level increased,and the mitochondrial membrane potential(MMP,ΔΨm)and Bcl-2/Bax ratio decreased(all P＜0.05).Compared with the MDL group,the cell survival rate of matsutake polysaccharide in the TMP-H group and the TMP-M group increased,the LDH release level decreased,the ΔΨm and Bcl-2/Bax ratio increased(P＜0.05),mitochondrial activity increased,the average length of mitochondrial network branches and the number of network branches increased,and the antagonistic membrane potential decreased(P＜0.05),among which the matsutake polysaccharide group was more obvious in the reduction of antagonistic membrane potential.Conclusion TMP have a protective effect against MPP+-induced PC12 cell damage,possibly by improving cell viability,reducing LDH release,antagonizing the reduction of mitochondrial membrane potential,and repairing mitochondrial network morphology,thereby reducing apoptosis.
万方数据
维普
