紫花牡荆素通过调节IL-10/STAT3信号通路减轻氧糖剥夺/复氧诱导的脑微血管内皮细胞损伤OA
Effect of casticin on oxygen-glucose deprivation/reoxygenation-induced brain microvascular endothelial cell injury by regulating IL-10/STAT3 signaling pathway
目的 探讨紫花牡荆素调节白细胞介素-10(IL-10)/信号转导及转录激活因子3(STAT3)通路对氧糖剥夺/复氧(OGD/R)诱导的脑微血管内皮细胞(BMEC)损伤的影响.方法 采用小鼠BMEC构建OGD/R损伤细胞模型,并分为OGD/R组、低浓度紫花牡荆素组、中浓度紫花牡荆素组、高浓度紫花牡荆素组、高浓度紫花牡荆素+AS101组,以未进行OGD/R诱导的细胞为对照组.采用MTT法测定细胞增殖;流式细胞术检测细胞凋亡;血管形成实验测定血管生成;Transwell小室检测跨内皮电阻(TEER);FITC葡聚糖检测内皮通透性;Western blotting检测BMEC中IL-10、p-STAT3和STAT3蛋白表达.结果 与对照组比较,OGD/R组BMEC细胞活性、TEER、IL-10和p-STAT3蛋白表达水平降低,管状结构形成减少,凋亡率和内皮通透性升高(P<0.05);与OGD/R组比较,低浓度紫花牡荆素组、中浓度紫花牡荆素组、高浓度紫花牡荆素组BMEC细胞活性、TEER、IL-10和p-STAT3蛋白表达水平升高,管状结构形成增加,凋亡率和内皮通透性降低(P<0.05);与高浓度紫花牡荆素组比较,高浓度紫花牡荆素+AS101组BMEC细胞活性、TEER、IL-10和p-STAT3蛋白表达水平降低,管状结构形成减少,凋亡率和内皮通透性升高(P<0.05).结论 紫花牡荆素通过调节IL-10/STAT3信号通路,减轻OGD/R诱导的BMEC损伤.
Objective To explore the effect of casticin on oxygen-glucose deprivation/reoxygenation(OGD/R)-induced brain micro-vascular endothelial cell(BMEC)injury by regulating interleukin-10(IL-10)/signal transducer and activator of transcription 3(STAT3)signaling pathway.Methods Mouse BMECs were used to establish an OGD/R cell model and divided into OGD/R,low-concentration casticin,medium-concentration casticin,high-concentration casticin,and high-concentration casticin+AS101 groups.BMECs without OGD/R induction were used as the control group.Cell proliferation was detected using the MTT assay,cell apoptosis using flow cytometry,angiogenesis using tube formation assay,transendothelial electrical resistance(TEER)using Transwell chambers,endothelial permeability using FITC-dextran assay,and the expression of IL-10,p-STAT3,and STAT3 proteins in BMECs using Western blotting.Results Com-pared with the control group,BMEC viability,tubular structure formation,TEER,and expression of IL-10 and p-STAT3 proteins were decreased in the OGD/R group,and the apoptosis rate and endothelial permeability were increased(P<0.05).Compared with the OGD/R group,BMEC viability,tubular structure formation,TEER,and expression of IL-10 and p-STAT3 proteins were increased in the low-,medium-,and high-concentration casticin groups,whereas the apoptosis rate and endothelial permeability were decreased(P<0.05).Compared with the high-concentration casticin group,BMEC viability,tubular structure formation,TEER,and expression of IL-10 and p-STAT3 proteins were decreased in the high-concentration casticin+AS101 group,and the apoptosis rate and endothelial permeability were increased(P<0.05).Conclusion Casticin may alleviate OGD/R-induced injury in BMECs by regulating IL-10/STAT3 signaling pathway.
唐永军;张煜华;玉山江·朱玛合;迪力木拉提·依斯热依力;西合热扎提·阿布力米提
新疆医科大学第二附属医院 重症医学科,乌鲁木齐 830011新疆医科大学第二附属医院 感染科,乌鲁木齐 830011新疆医科大学第二附属医院 重症医学科,乌鲁木齐 830011新疆医科大学第二附属医院 重症医学科,乌鲁木齐 830011新疆医科大学第二附属医院 重症医学科,乌鲁木齐 830011
医药卫生
紫花牡荆素白细胞介素-10信号转导及转录激活因子3氧糖剥夺/复氧脑微血管内皮细胞
casticininterleukin-10signal transducer and activator of transcription 3oxygen-glucose deprivation/reoxygenationbrain microvascular endothelial cell
《中国医科大学学报》 2026 (5)
437-442,6
自治区重点实验室新疆神经系统疾病研究重点实验室开放课题(XJDX1711-2405)
评论