探讨缺氧复给氧损伤后脑微血管内皮细胞凋亡的机制。
To explore the mechanism of apoptosis after hypoxia-reperfusion oxygen damage the cerebral microvascular endothelial cells.
目的探讨麦冬药物血清抗血管内皮细胞凋亡的分子机制。
OBJECTIVE to investigate into the molecular mechanism of the pharmacological serum of Radix Ophiopogonis against the apoptosis of vascular endothelial cell.
探讨慢性增强型体外反搏对高胆固醇血症猪主动脉血管内皮细胞凋亡的影响。
Objective To explore the effect of long-term enhanced external counterpulsation(EECP)on apoptosis of vascular endothelial cells in the aorta of hypercholesterolemic pigs.
结果细胞因子、辐射、氧自由基等可诱导血管内皮细胞凋亡，导致血管损伤；
Results Cytokine, radiation could induce apoptosis of endothelial cells, and caused vascular damage.
HCY在生理浓度铜离子存在下可能通过氧化应激损伤的机制而导致血管内皮细胞凋亡。
The apoptosis in vascular endothelial cells induced by HCY plus copper was involved in the mechanism of oxidative stress-mediated injury.
目的观察高葡萄糖和高软脂酸联合应用对人血管内皮细胞凋亡的作用效果，并探讨其机制。
Objective To evaluate the apoptosis effectiveness and the mechanism of combined use of high glucose with high palmitic acid on human vessel endothelial cells.
结论：APC拮抗lps诱导的血管内皮细胞凋亡并促进细胞的增殖，发挥保护细胞的作用。
CONCLUSION: APC can inhibit HUVECs apoptosis induced by LPS and promote cell proliferation, thus protect the cells from injury.
而小叶间胆管周围小血管内皮细胞的损伤可能是导致小叶间胆管上皮细胞凋亡的直接原因。
The apoptosis of the epithelial cells may be related to the damage of interlobular bile ducts.
目的：从脂多糖(LPS)所致血管内皮细胞(vec)凋亡的角度进行了实验研究，为进一步探讨血瘀证实质及分子机制。
Objective: the apoptosis of human umbilical vascular endothelial cell (HUVEC) was induced by lipopolysaccharide (LPS) in order to explore syndrome of blood stasis and its molecular mechanism.
目的探讨氧合血红蛋白对体外培养的大鼠脑微血管内皮细胞增殖和凋亡的影响。
Objective to investigate the effect of oxyhaemoglobin on proliferation and apoptosis of cultured rat brain microvascular endothelial cells.
目的研究苯磷硫胺对体外高糖环境中培养的牛视网膜毛细血管内皮细胞的生长及细胞凋亡的影响。
The purpose of this paper was to study the effect of benfotiamine on proliferation and apoptosis of bovine retinal capillary endothelial cells cultured in high concentration of glucose.
所观察的几种肿瘤中的微血管内皮细胞孔窗及内皮细胞裂隙与转染的目的基因无明显的关系，且内皮细胞的凋亡均不明显。
No correlation between gene transfection and fenestra formation or cleft of capillary endothelial cells was observed, and no apoptosis of endothelial cells was found.
RAS抑制可以通过多种分子机制抑制肺泡上皮细胞和血管内皮细胞的凋亡，抑制炎症级联反应和细胞外基质沉积，而使肺纤维化病变减轻。
RAS inhibition can reduce cell apoptosis of alveolar epithelial cells and endothelial cells, interfere with the inflammation cascade, and decrease fibroblast activity during tissue repair process.
脑微血管内皮细胞缺氧复给氧损伤后，采用流式细胞仪检测细胞凋亡的程度。
Apoptosis was detected with flow cytometry after hypoxia-reperfusion oxygen damage of the cerebral microvascular endothelial cells.
结论舒林酸的硫化代谢产物能够显著抑制血管内皮细胞的增殖活性，改变细胞的周期分布，使细胞阻滞于G 2期，并可能在此期诱导其凋亡。
Conclusions Sulfide can significantly reduce the proliferation of ECV304, change the cell cycle distribution and arrest cells in G2-M phase where apoptosis may be induced.
结论舒林酸的硫化代谢产物能够显著抑制血管内皮细胞的增殖活性，改变细胞的周期分布，使细胞阻滞于G 2期，并可能在此期诱导其凋亡。
Conclusions Sulfide can significantly reduce the proliferation of ECV304, change the cell cycle distribution and arrest cells in G2-M phase where apoptosis may be induced.
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