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作 者:杜旌畅 程青青 母昌会 Du Jingchang;Cheng Qingqing;Mu Changhui(School of Public Health,Chengdu Medical College,Chengdu,Sichuan 610500,China)
机构地区:[1]成都医学院公共卫生学院,四川成都610500
出 处:《四川医学》2020年第5期463-467,共5页Sichuan Medical Journal
基 金:四川省卫生和计划生育委员会科研课题(编号:18PJ582)。
摘 要:目的探索藁本内酯对于缺血状态下血管内皮细胞的促增殖作用及其机制。方法以人脐静脉内皮细胞(HUVEC)为研究对象,细胞被分为对照组、氧糖剥夺(OGD)造模组、给药组以及抑制剂组;CCK-8法检测细胞活性;划痕实验与成血管实验检测细胞迁移及成血管能力;Western blot法测定细胞中PI3K-p85、总Akt、p-Akt、HIF-1α、VEGF及VEGFR 2的表达。结果与对照组比较,模型组细胞活性与细胞成血管能力下降,差异有统计学意义(P<0.05),细胞迁移能力及PI3K-p85、p-Akt表达无明显变化,差异无统计学意义(P>0.05),HIF-1α、VEGF及VEGFR 2的表达则显著上升,差异有统计学意义(P<0.05);给予藁本内酯后,与模型组相比,给药组细胞活力、细胞迁移能力、细胞成血管能力以及相关细胞因子的表达均升高,差异有统计学意义(P<0.05),在予以LY294002后,与给药组比较,除VEGFR 2外所有指标均出现明显下降,差异有统计学意义(P<0.05)。结论藁本内酯具有明确的促进体外模拟缺血环境下血管新生的能力,该能力与PI3K-Akt通路的激活有关。Objective To explore the effect of ligustilide on the proliferation of vascular endothelial cells under ischemia and its mechanism.Method Human umbilical vein endothelial cells(HUVEC)was taken as the research object,cells were divided into four groups:control group(CG),model group(MG)by oxygen glucose deprivation(OGD),treatment group(TG)by drug administration and inhibitor group(IG).CCK-8 method was used to detect cell activity.Angiogenesis test was used to detect cell migration and angiogenesis ability.Western blot was used to determine the expression of PI3K-p85,total Akt,p-Akt,HIF-1α,VEGF and VEGFR2 in cells.Result Compared with CG,the cell activity and angiogenic ability of MG decreased(P<0.05),the cell migration ability and PI3K-p85,p-Akt expression had no significantly changes(P>0.05),the expression of HIF-1α,VEGF and VEGFR2 increased significantly(P<0.05).After giving ligustilide,compared with MG,the cell viability,cell migration ability,cell angiogenic ability and expression of related cytokines in TG were all increased(P<0.05).After giving LY294002,compared with TG,all indexes except VEGFR2 showed a significant decrease(P<0.05).Conclusion Ligustilide has a clear ability to promote angiogenesis in vitro in a simulated ischemic environment,which is related to the activation of PI3K-Akt pathway.
分 类 号:R331.3[医药卫生—人体生理学]
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