目的探讨姜黄素对大鼠局灶性脑缺血再灌注损伤后的基质金属蛋白酶-9(MMP-9)及MMP-2表达及活性的影响。方法采用线栓法制作大鼠暂时性大脑中动脉栓塞(MCAO)模型,MCAO后1h腹腔注射100mg/kg姜黄素,MCAO2h再灌注22h后处死动物。取患侧或对照侧端脑,提取总蛋白,采用Western blot和明胶酶谱分析方法研究MMP-9及MMP-2的表达及活性。结果 Western blot和明胶酶谱分析结果均表明,姜黄素可降低脑缺血再灌注损伤所诱导的MMP-9及MMP-2蛋白的表达及其活性水平。结论姜黄素对脑缺血再灌注损伤的保护作用机制之一可能与抑制了MMP-9及MMP-2蛋白的高表达及活性增高有关。
Objective To determine whether sulforaphane （SFN） protects neurons against injury caused by oxygen-glucose deprivation/reoxygenation （OGD/R） and, if so, to investigate the possible mechanisms. Methods Primary cultures of neurons were prepared from the cerebral cortex of 1-day-old Sprague-Dawley rats. On days 5-6 in vitro, the neurons were exposed to OGD for 1 h, followed by reoxygenation for 24 h. Cells were treated with 0, 0.1, 0.2, 0.5, 1, 2.5, or 5 μmol/L SFN, with or without 10 μmol/L LY294002, a PI3K-specific inhibitor, during OGD/R （a total of 25 h）. After 24-h reoxygenation, MTT was used to assess viability and injury was assessed by Hoechst 33258/propidium iodide （PI） staining; immunofluorescence staining and Western blot were performed to detect molecular events associated with apoptosis. Results The MTT assay showed that 1 μmol/L SFN significantly increased viability, and Hoechst 33258/PI staining showed that the numbers of injured neurons were reduced significantly in the SFN group. Furthermore, immunofluorescence staining and Western blot showed that SFN increased Bcl-2 and decreased cleaved caspase-3 levels. Moreover, LY294002 inhibited the phosphorylated-Akt expression evoked by SFN, decreased Bcl-2 expression and increased cleaved caspase-3 expression. Conclusion SFN protects neurons against injury from OGD/R and this effect may be partly associated with an anti-apoptosis pathway.
