枸杞多糖通过下调miR-23a减轻顺铂诱导的颗粒细胞损伤

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Abstract：ObjectiveToevaluatetheprotectiveefectofLyciumbarbarumpolysaccharides （LBP）against cisplatin-induced ovariangranulosacellinjuryand investigateitsposible mechanisms.MethodsHuman granulosa-liketumorcelline （KGN） weretreatedwith 2.5μg/mL cisplatin for 24h， followedbytreatmentwith100，500，and 1000mg/L LBP，and the changes in cell viability，apoptosis，levelofnti-Mullrianormone （AMH），andcellultrastructure wereetectedwithCCK-8assayflow cytometryEdssoeoapoofe3lpathway proteins wereanalyzedusing Westernbloting，andthe expressionofmiR-23a wasdetected withRT-qPCR.KGNcell modelswithlentivirus-mediated miR-23aoverexpresionor knockdownwereusedtoverifythetherapeuticmechanismof LBP.ResultsCsplatintreatmentsigniicantlyinibitedcellibilityinducedapoptosis，ecreasedAMHlevelused ultrastructualoliseaddsps3ssodlwdcl-eioinc.a alsosuppressed theactivationof thePI3K/AKTsignaling pathwayandupregulated miR-23aexpression in thecels.LBP interventionoiouslyllviatedcisplatiducedjusinelsndinartilaLtreamentattemimoe for24hsignicantlyiproedGcellviabilityducedapotosisancedteirdocinefunctinnlite ultrastructural abnormalities.Mechanisticall，medium-doseLBPobviouslyactivatedthePI3K/AKTpathwayby downregulatingmiR-23aincisplatin-treatedcels，subsequentlyinhibiting Baxandcaspase-3whileupregulatingBcl-2. Overexpresion of miR-23a weakenedwhile knockdown of miR-23a significantly enhanced the protective effectsof LBP. ConclusionLBPaleviates cisplatin-inducedapoptosis in KGNcells byinibitingmR-23aexpressionandactivatingthe PI3K/ AKT pathway， suggesting a potential therapeutic strategy for ovarian function preservation.

Keywords：Lyciumbarbarumpolysaccarides;miR-23a;KGNcels;cellapoptosis;PI3K/AKTsignalingpathw

枸杞多糖（LBP）是传统中药枸杞子中具有较高提取、利用价值的活性成分，具有抗炎、抗氧化、抗衰老、生殖保护、神经保护、免疫调节等多种药理作用[1]。（剩余17488字）