Aim This study was to evaluate the effect of arsenic trioxide （As2O3） on the transgenic TNF-α promoter activity in cultured vascular smooth muscle cells （VSMCs） and THP-1 monocytes. Methods Human TNF-α promoter ...
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Aim This study was to evaluate the effect of arsenic trioxide （As2O3） on the transgenic TNF-α promoter activity in cultured vascular smooth muscle cells （VSMCs） and THP-1 monocytes. Methods Human TNF-α promoter was constructed by reporter gene system and was transiently transfected into VSMCs and THP-1 in vitro. The promoter activity was tested by luciferase activity with or without LPS and Ang Ⅱ stimulation, before and after different dosage of As2O3 treatment. Results 1. TNF-α promoter effectively expressed in VSMCs and THP-1 compared with CMV promoter （58.3% and 80.9%, respectively）. Both LPS and Ang Ⅱ significantly up-regulated TNF-α promoter activity （P〈0.05）. 2. As2O3 significantly inhibited, both intact and LPS/Ang Ⅱ stimulated promoter activity, in a dose dependent manner （P〈0.05）, and in both cell type. Conclusion These results manifested that, the inhibition effect of As2O3 on the activity of human TNF-α promoter indicated its potential inhibition on pro-inflammatory cytokine genes expression at transcriptional level and its potential anti-inflammatory property in the cardiovascular system.
目的探讨人脑梗死灶周围组织星形胶质细胞和微血管的变化。方法应用9例因脑梗死而死亡尸检全脑标本,常规 HE 和免疫组织化学染色(SP)标记星形胶质细胞中的胶质纤维酸性蛋白(GFAP)和微血管标记物(CD31),观察星形胶质细胞和微血管的变化...
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目的探讨人脑梗死灶周围组织星形胶质细胞和微血管的变化。方法应用9例因脑梗死而死亡尸检全脑标本,常规 HE 和免疫组织化学染色(SP)标记星形胶质细胞中的胶质纤维酸性蛋白(GFAP)和微血管标记物(CD31),观察星形胶质细胞和微血管的变化规律。结果以梗死灶为中心,由内到外可分4个区(0～3区);GFAP 在0区和1区表达很少,在2区和3区随缺血时间延长表达持续升高;CD31在0区无表达,在1区可见少量表达,在2区和3区随缺血时间延长表达持续升高。结论脑梗死后星形胶质细胞和微血管反应性增生,在缺血后期 GFAP、CD31广泛表达,两者在组织损伤修复重建过程中起重要作用。
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