It is difficult to control the degree of ischemic postconditioning in the brain and other isch-emia-sensitive organs. Remote ischemic postconditioning could protect some ischemia-sensitive organs through measures on terminal organs. In this study, a focal cerebral ischemia-reperfusion injury model was established using three cycles of remote ischemic postconditioning, each cycle consisted of 10-minute occlusion of the femoral artery and 10-minute opening. The results showed that, remote ischemic postconditioning signiifcantly decreased the percentage of the in-farct area and attenuated brain edema. In addition, inlfammatory nuclear factor-κB expression was signiifcantly lower, while anti-apoptotic Bcl-2 expression was signiifcantly elevated in the ce-rebral cortex on the ischemic side. Our ifndings indicate that remote ischemic postconditioning attenuates focal cerebral ischemia/reperfusion injury, and that the neuroprotective mechanism is mediated by an anti-apoptotic effect and reduction of the inlfammatory response.

Amentoflavone is a natural biflavone compound with many biological properties, including anti-inlfammatory, antioxidative, and neuroprotective effects. We presumed that amentolfavone exerts a neuroprotective effect in epilepsy models. Prior to model establishment, mice were intragastrically administered 25 mg/kg amentoflavone for 3 consecutive days. Amentoflavone effectively prevented pilocarpine-induced epilepsy in a mouse kindling model, suppressed nu-clear factor-κB activation and expression, inhibited excessive discharge of hippocampal neurons resulting in a reduction in epileptic seizures, shortened attack time, and diminished loss and apoptosis of hippocampal neurons. Results suggested that amentolfavone protected hippocampal neurons in epilepsy micevia anti-inlfammation, antioxidation, and antiapoptosis, and then ef-fectively prevented the occurrence of seizures.

孕激素在子痫前期患者TLR4-MyD88依赖的信号通路中的作用

目的 研究孕激素在子痫前期(preeclampsia,PE)孕妇Toll样受体4(toll-like receptor4,TLR4)-髓样细胞分化蛋白88(myeloid differentiation factor 88,MyD88)依赖的信号通路中的作用.方法 原代培养子痫前期孕妇外周血单个核细胞(peripheral blood mononuclear cell,PBMC),以不同浓度孕激素(0 mol/L、10-8 mol/L、10-6mol/L、 10-4mol/L)处理,实时定量聚合酶联反应(Real-time polymerase Chain reaction,real-time PCR)检测TLR4 mRNA、MyD88 mRNA、核转录因子-κB (nuclear factor κB,NF-κB) mRNA的表达;免疫印迹法Western blot检测IκB-α蛋白的表达,用凝胶图像处理系统分析各条目标带灰度值酶联免疫吸附试验(Enzyme-linked immunosorbent assay,ELISA)检测细胞上清液中肿瘤坏死因子-α (tumor necrosis factors,TNF-α)及白介素-6(interleukin-6,IL-6)的表达.结果 随着孕酮浓度的增加,各组TLR4 mRNA、MyD88 mRNA及NF-κB mRNA的相对表达量2-△△Ct均逐渐降低,IκB-α蛋白的表达逐渐增加,差异均有统计学意义(均P<0.05);同时,细胞上清液中细胞因子TNF-α及IL-6的表达均逐渐减少,差异均有统计学意义(P<0.05).结论 孕激素可显著抑制TLR4-MyD88依赖的信号传导通路,对子痫前期患者具有保护作用.