黄芩素通过抑制JAK2/STAT1通路减轻Aβ25-35诱导的PC12细胞损伤

Baicalein reduces Aβ-induced PC12 cell damage by inhibiting the JAK2/STAT1 pathway

本研究旨在探讨黄芩素对Aβ25-35诱导PC12细胞损伤的保护作用及机制。采用20μmol·L-1 Aβ25-35损伤PC12细胞,通过细胞形态观察、Hoechst 33342染色和炎症因子检测考察黄芩素对Aβ25-35损伤PC12细胞的保护作用,采用Western blotting方法检测凋亡相关蛋白半胱氨酸天冬氨酸蛋白酶3(cysteinyl aspartate specific proteinase 3,caspase-3)、活化型半胱氨酸天冬氨酸蛋白酶3(cleaved cysteinyl aspartate specific proteinase-3,cleaved caspase-3)、Janus激酶2/信号转导子和转录激活子1(Janus kinase 2/signal transducer and activator of transcription 1,JAK2/STAT1)通路相关蛋白及其下游一氧化氮合酶(inducible nitric oxide synthase,iNOS)和环氧合酶-2(cyclooxygenase-2,COX-2)炎症蛋白的表达,研究黄芩素的作用机制。结果显示,黄芩素(80μmol·L^(-1))能显著抑制Aβ25-35诱导的PC12细胞凋亡和炎症因子IL-8和TNF-α的释放;Western blotting实验结果显示,黄芩素能抑制JAK2和STAT1的磷酸化,并抑制其下游蛋白iNOS和COX-2的表达。以上结果表明,黄芩素能有效抑制JAK2/STAT1信号通路,从而抑制Aβ25-35诱导的PC12细胞损伤。

This study investigated the mechanism by which baicalein protected PC12 cells from Aβ25-35-induced injury.PC12 cells were treated with Aβ25-35(20μmol·L-1)and the ability of baicalein to prevent apoptosis was investigated by monitoring changes in cell morphology,Hoechst 33342 staining,and measurement of inflammatory factors.Western blotting was used to detect the expression of the apoptosis-related proteins cysteinyl aspartate specific proteinase-3(caspase-3),cleaved cysteinyl aspartate specific proteinase-3(cleaved caspase-3),proteins involved in the Janus kinase 2/signal transducer and activator of transcription 1(JAK2/STAT1)pathway,and downstream inducible nitric oxide synthase(iNOS)and cyclooxygenase-2(COX-2).The results show that baicalein(80μmol·L^(-1))can significantly inhibit apoptosis and the release of inflammatory factor IL-8 and TNF-αin Aβ25-35-treated PC12 cells.Western blotting results showed that baicalein can inhibit the phosphorylation of JAK2 and STAT1 and decrease the expression of downstream iNOS and COX-2,thereby inhibiting the JAK2/STAT1 signaling pathway and preventing Aβ25-35-induced PC12 cell damage.