白细胞介素6、肿瘤坏死因子对体外培养的血管内皮细胞的损伤作用

目的：研究白细胞介素６（ＩＬ－６）和肿瘤坏死因子（ＴＮＦ）对人脐静脉内皮细胞（ＨＶＥＣ）的损伤作用。方法：以原代培养的ＨＶＥＣ为模型，将ＩＬ－６、ＴＮＦ及其抗体与ＨＶＥＣ共同孵育，观察内皮细胞（ＥＣ）形态变化和培养液中血管紧张素转化酶（ＡＣＥ）和乳酸脱氢酶（ＬＤＨ）水平。结果：ＴＮＦ和ＩＬ－６可引起细胞间隙增大，甚至细胞脱落；并且随着ＴＮＦ和ＩＬ－６浓度加大及作用时间延长，培养液中ＡＣＥ和ＬＤＨ水平升高。

肿瘤坏死因子引起的内皮细胞损伤与C－jun基因表达的变化

肿瘤坏死因子引起的内皮细胞损伤与Ｃ－ｊｕｎ基因表达的变化ＤａｍａｇｅｏｆＥｎｄｏｔｈｅｌｉａｌＣｅｌｌｓＩｎｄｕｃｅｄｂｙＴＮＦａｎｄＣｈａｎｇｅｏｆｃ－ｊｕｎＧｅｎｅＥｘｐｒｅｓｓｉｏｎ￥／／文／金惠铭，沙志一微血管壁通透性升高是创伤、感染、休克等...

Effect of Anti-KDR Antibody on the Proliferation of Hemangioma Vascular Endothelial Cells in vitro

The suppressive effect of anti-KDR antibody against VEGF on proliferation of hemangioma-derived vascular endothelial cells （HVECs） was investigated. HVECs from one case of hemangioma in proliferative phase were cultured. Both primary culture and sub-culture were conducted in M199 medium. The HVECs of passage 3 were divided into 4 groups based on the concentrations of anti-KDR antibody. Cell count was performed and inhibitory rate of HVECs was measured before and 9 days after interference. The results showed that the number of HVECs in the anti-KDR anti- body-treated groups was significantly decreased and the inhibitory rate of HVECs by anti-KDR antibody （50, 10 and 2 μg/mL） was 84%, 63% and 39% respectively at 9th day after interference, with the difference being significant. In the control group, the number of HVECs was increased significantly. In was concluded that the anti-KDR antibody could suppress the activity of VEGF through blocking the KDR, indicating the potential clinical applications of anti-KDR antibody in the treatment of hemangioma.

The impact on secreted VEGF of Hep-2 human laryngeal cancer cell induced by Rg3

Objective：The aim of this study was to investigate the af ecting of Rg3 to secreted VEGF of human laryngeal carcinoma Hep-2 cells and its mechanism of inhibition to tumor angiogenesis. Methods：Cultured human laryngeal cancer cellline Hep-2 and human vascular endothelial cells in vitro, cells got into the period of exponential phase of growth, was diviced into 3 groups：group I （control group）, group II （DDP group）, group III （Rg3 group）. Added to the Hep-2 cells Rg3 and DDP, made Rg3 final concentration was 300μg/mL, and DDP was 3μg/mL. 48 h later, specimens from sample to be done immunocytochemistry, and the protein of VEGF in Hep-2 cells to be detected. Col ecting Hep-2 cells supernatant, some was used to measure the protein level of VEGF in Hep-2 cells supernatant by ELISA. Some was used to culture HVEC. 24 h later, cellgrowth inhibition rate of human vascular endothelial was determined by MTT. Results：The protein level of VEGF was evi-dently higher in group I compared to group II and group III, it was not only in Hep-2 cells, but also in supernatant of Hep-2 cells. There was no significantly dif erent between group II and group III. MTT results showed that, the human vascular endothelial cellgrowth inhibition rate of group I was significantly lower than that of group II and group III （P〈0.05）. At the same time the HVEC growth inhibition rate of group II was significantly lower than that of group III （P〈0.05）. Conclusion：The inhibition to tumor angiogenesis of Rg3 is stronger than traditional chemotherapy drug cisplatin. It worke by reducing the biological ef ects of secreted VEGF, But the ef ecting worke by reducing the activity of secreted VEGF itself or af ecting endothelial function of VEGF receptor or some other ways to be further studied.

雌激素和血管内皮细胞生长因子促进血管瘤增殖的体外实验研究

目的 研究雌二醇 (E2 )和血管内皮细胞生长因子 (VEGF)在促进血管瘤血管内皮细胞(HVEC)增殖中的作用和相互关系 ,以及 4羟基他莫昔芬 (4OH TAM )对该促进作用的影响。方法 取 2例雌激素受体阳性的皮肤增生期草莓状血管瘤标本 ,采用组织块培养法培养HVEC。HVEC原代及传代培养在M 199培养液中进行 ,传至第三代时改用无雌激素培养液IMEM进行干预实验 ,实验分 5组 :组 1(无干预 ,为对照组 )、组 2 (加E2 )、组 3(加VEGF)、组 4 (加E2 和VEGF)、组 5 (加E2 、VEGF和 4OH TAM )。分别在 0、3、6、9d进行细胞计数 (CC)和流式细胞仪DNA增殖指数 (PI)检测。结果 例 1在第 9d时 ,组 2示HVEC轻微增殖 ,CC和PI分别为组 1的 1.38倍和 1.6 1倍 ;组 3示CC及PI明显增加 ,分别为组 2的 2 .10倍和 1.6 1倍 ;组 4示CC及PI的增加更加显著 ,分别是组 3的 1.6 2倍和 1.4 0倍 ;组 5的CC和PI与组 1相仿。例 2的实验结果与例 1相似。结论 体外实验显示雌激素能够轻微促进HVEC增殖 ;VEGF可明显促进HVEC增殖 ;而雌激素和VEGF同时存在时 ,对HVEC的促增殖作用更加显著 ,二者存在协同作用 ;他莫昔芬能抑制这种协同促增殖作用。