目的研究苏合香对小鼠脑微血管内皮细胞(b End.3)的保护作用。方法空白对照组给予DMEM培养基于孵箱中正常培养24 h;模型组予以氧糖剥夺8 h/复氧16 h;实验A、B、C、D组分别予以10,50,100,200μg·mL^-1苏合香培养24 h后,再予以氧糖剥夺8 h/复氧16 h。用细胞增殖与活性检测试剂盒和均质膜完整性检测试剂盒检测细胞活力和乳酸脱氢酶(LDH)释放量,用酶联免疫吸附法检测b End.3上清液中肿瘤坏死因子-α(TNF-α)和细胞间黏附分子-1(ICAM-1)的含量。结果与空白对照组比较,模型组细胞活力明显降低,LDH释放量和细胞上清液中TNF-α和ICAM-1的含量均明显升高(P〈0.05)。与模型组比较,实验A、B、C、D组细胞活力明显升高,LDH释放量明显减少,细胞上清液中TNF-α和ICAM-1的含量不同程度地降低(P〈0.05)。结论苏合香能够改善氧糖剥夺/复氧诱导的脑微血管内皮细胞的损伤,其机制可能是通过降低相关炎症因子的表达而发挥脑保护作用。
Objective To investigate the protective effects of storax on brain microvascular endothelial cells(bEnd. 3). Methods Cultured brain microvascular endothelial cells b End. 3 were divided into the control group, model group [oxygen- glucose deprivation(OGD)8 h / reoxygenation(R) 16 h],and test A,B,C,D groups with 10,50,100,200 μg·mL^-1 storax preconditioning 24 h,then OGD 8 h / R16 h. The cell viability and lactate dehydrogenase(LDH) release were evaluated by cell counting kit-8 assay and Cyto Tox- ONE^TM Homogeneous Membrane Integrity Assay respectively. Then enzyme linked immunosorbent assay( ELISA) was used to detect the content of tumor necrosis factor- α( TNF- α) and intercellular cell adhesion molecule- 1(ICAM-1) in the cell supernatant. Results Compared with the control group, the cell viability of model group decreased significantly,the LDH release and TNF- α,ICAM-1 expression increased significantly after OGD / R injury( P〈0. 05). Compared with the model group,storax could increase the cell viability,decrease the release of LDH,and reduce the content of TNF- α,ICAM- 1 in cell supernatant( P〈0. 05). Conclusion Storax has protective effects on the brain microvascular endothelial cells damage induced by OGD / R,and themechanism may be related to the decrease of the expression of inflammatory cytokine.