脑出血继发损伤中沉默信息调节因子2的表达和炎症反应*

目的：探讨脑出血对酵母沉默信息调节因子2（Sirt2）和炎症的影响。方法：将胶原酶Ⅳ注入SD大鼠右侧 纹状体中建立脑出血模型，通过免疫印迹和ELISA 等方法测定大鼠脑出血后48 h 的Sirt2 的表达及炎症变化。利 用Hemin 诱导PC12 细胞损伤模拟体外脑出血模型，并检测Sirt2 及炎症变化；采用短发夹RNA（shRNA）-Sirt2 沉 默Sirt2 在PC12 细胞中的表达及对炎症的影响。结果：手术后48 h 脑出血行为学评分最低。脑出血组Sirt2 的表达 显著高于假手术组。脑出血组IL-6、IL-1β 表达显著升高。结论：脑出血可以促进Sirt2 的表达和炎症反应，降低 Sirt2 的表达可减缓炎症反应。 关键词 脑出血；沉默信息调节

Protective effect of propofol combined with midazolam on PC12 cells in cerebral ischemia-reperfusion model

Objective To investigate the molecular mechanism of protective effect of propofol（PPF） combined with midazolam（MID） on PC12 cells in constructed oxygen glucose deprivation （OGD）model. Methods PC12 cells were treated with glucose free medium and an aerobic environment （5% CO2 and 95% N2） to construct OGD model. OGD model cells were treated with PPF， MID or PPF+MID ；besides， miR-103-3p mimics， miR-103-3p inhibitor， si-prostaglandin-endoperoxide synthase 2（PTGS2）， pcDNA-PTGS2 or miR-103-3p mimics+pcDNAPTGS2 were transfected into PC12. Cell proliferation was detected by CCK-8 ； apoptosis rate was measured by flow cytometry. Ca2+ level was detected by Fura-2/AM fluorescence assay ；expression of miR-103-3p was measured by RT-qPCR. Expression of apoptosis related proteins （Bcl-2， Bax， c-caspase-3 and c-caspase-9）， and PTSG2 were detected by Western blotting. The relationship between miR-103-3p and PTGS2 was confirmed by dual-luciferase reporter gene assay system. Results PPF combined with MID increased the proliferation， decreased apoptosis and Ca2+ level of PC12 in OGD model. Additionally， it also markedly up-regulated the expression of miR-103-3p in PC12. Moreover， miR-103-3p target down-regulated the protein level of PTGS2 in PC12. Overexpression of miR- 103-3p and silencing of PTGS2 alleviated the injury of PC12 cells induced by OGD， and knockdown of miR-103-3p and overexpression of PTGS2 aggravated the injury of PC12 in OGD model. Conclusion PPF combined with MID alleviates injury of PC12 cell in OGD model by up-regulating miR-103-3p and inhibiting PTGS2.