黄芪甲苷通过抑制PINK/Parkin通路调控细胞线粒体自噬减轻D-半乳糖诱导的内皮细胞衰老

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Abstract：ObjectiveToexplorethemechanismbywhichastragalosideIV（AS-IV）aleviatesD-galactose （D-GAL）-induced senescence inhuman umbilical vein endothelialcells （HUVECs）.Methods Cultured HUVECs were treated with D-GAL （40g/L） 、 AS-IV （200μmol/L） D-GAL+AS-IV，or D-GAL+AS-IV+MTK458 （amitochondrial autophagyagonist， 25μmol/L ）for 48h， and thechangesincelloliferaionigrationnngigenesispacityeealuated.Cellotosis，activegesie （ROS）levels，oorialmembrnepotetialadexpreionsofutoag-related proteis（LC3-/C3-）dK1/ Parkinpathwayproteinsinthetreatedcelsweredetected.ResultsAS-IVtreatmentsignificantlyreducedtheinhibitoryefect ofD-GALonHUVECviabilityefectivelyallviatedD-GAL-inducedimpairmentoftubeformingabilityandprooted angiogenesisand migrationabilityof thecels.AS-IValsosignificantlyreducedtherateofD-GAL-induced HUVECs positive forsenescence-associated β -galactosidase（SA- β -Gal） staining and inhibited the expressionof senescence-related genesP21and P53.AS-IVrestoredmitochondrialmembrane potentialandreduced intracelularROSlevels inD-GAL-inducedHUVECs，and inhibitedthefusionof autophagosomesandlysosomes to prevent thecompletionof autophagicflux.InHUVECstreated with bothD-GALand AS-IV，theapplication MTK458significantlyincreasedthenumberof yellowspotsandenhanced the expressiosofei.l senescence by inhibiting the PINK1/Parkin pathway to regulate mitochondrial autophagy.

Keywords：astragaloside; PINK1/Parkinsignaling pathway;mitochondrialautophagy;D-galactose;endothelialcels;cellar senescence

细胞衰老，作为生物体老化的核心机制之一，近年来其作为慢性疾病驱动因素的病理学价值受到深度关注。（剩余17164字）