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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 study the protective effect of Su-Hsiang on mouse brain microvascular endothelial cells (b-End.3). Methods The blank control group was given DMEM culture medium for 24 hours in normal incubator; the model group was given oxygen deprivation for 8 hours / reoxygenation for 16 hours; the rats in groups A, B, C and D were treated with 10,50,100,200 μg · mL - 1) Sulpacas cultured for 24 h, then oxygen deprived 8 h / reoxygenation 16 h. Cell viability and lactate dehydrogenase (LDH) release were measured by cell proliferation and activity assay kit and homogeneity membrane integrity assay kit. The levels of TNF-α, α (TNF-α) and intercellular adhesion molecule-1 (ICAM-1) levels. Results Compared with the blank control group, the viability of the model group was significantly decreased, and the release of LDH and the levels of TNF-α and ICAM-1 in the supernatant of the model group were significantly increased (P <0.05). Compared with the model group, the cell viability of the experimental groups A, B, C and D were significantly increased, and the release of LDH was significantly reduced. The contents of TNF-α and ICAM-1 in the supernatant decreased to some extent (P <0.05). Conclusion Su Hexiang can improve the injury of cerebral microvascular endothelial cells induced by oxygen deprivation and reoxygenation. Its mechanism may be that it can protect cerebral microvascular endothelial cells by decreasing the expression of related inflammatory cytokines.