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作 者:郄福忠[1] 刘兴吉[2] 鞠砚[2] 李毅平[2] 李蕴潜[2]
机构地区:[1]大庆油田总医院神经外科,黑龙江大庆163001 [2]吉林大学第一临床医学院神经外科,吉林长春130021
出 处:《中华肿瘤防治杂志》2006年第6期442-444,共3页Chinese Journal of Cancer Prevention and Treatment
摘 要:目的:研究金丝桃素被光激活后对C6胶质瘤的抑制作用及其对bFGF、bFGF-R和微血管密度(microvesseldensity,MVD)的影响。方法:将接种C6胶质瘤细胞后的40只Wistar大鼠随机分为5组,空白对照组、高和低剂量金丝桃素作用组、高和低剂量金丝桃素+光照组,16d后切取肿瘤组织,称质量计算抑瘤率,标本用SP法免疫组化染色,检测瘤组织中bFGF、bFGF-R和MVD。结果:1)光照下,当金丝桃素为0·8μg/mL时,抑瘤率为67·2%,金丝桃素为2·0μg/mL时抑瘤率为82·4%,非光照金丝桃素组对肿瘤无抑制作用。2)bFGF在各组大鼠C6胶质瘤组织中均有表达,表达值较高,各组间差异无统计学意义。空白对照组中bFGF-R表达较高,且微血管计数最多。金丝桃素+光照组中bFGF-R蛋白表达和MVD明显低于非光照组及对照组,P=0·019,P=0·007,呈剂量依赖关系。bFGF-R与肿瘤MVD呈正相关,rbFGF-R=0·85。结论:光激活金丝桃素对bFGF-R有抑制作用,对bFGF表达没有影响。光激活的金丝桃素能抑制大鼠C6胶质瘤生长的机制,可能是抑制肿瘤组织中bFGF-R后,阻止了bFGF发挥效应,抑制了肿瘤间质血管生成,而抑制肿瘤的生长。OBJECTIVE: To study the therapeutic function and mechanism about photo-activated hypericin to rat C6 glioma. METHODS: First, C6 glioma auto-transplanted animal models were established, then different doses of hypericinwere used to act on the models under light or no light. After 16 days, tumors were removed and dealed with immunohistochemistry. Finally, the resuits were analysed with the statistic methods. RESULTS: 1) The effect of hypericin showed a trait of doseage-dependent in inhibiting the growth of glioma under light, and it inhibited 67.2% of tumors at 0.8 μg/mL, and 82.4% at 2.0 μg/mL. The tumor's weight in the group of high dosage was significantly lower than that in the group of low dosage, P=0.019,P=0.007. 2) There was a high protein expression of bFGF in every group. The expression of bFGF-R was high in the control group. Their expression of HY+ light group was lower than that of the group of control and of no light, and MVD was the same. There was a positive relationship between bFGF-R's protein and tumor interstitial MVD, r=0.85. CONCLUSIONS: Hypericin can effectively inhibit the growth of C6 glioma under light. Hypericin+light significantly refrains the expression of bFGF-R in the level of protein. However there is no effect on protein expression of bFGF. Photoactivated hypericin may inhibit bFGF receptor and tumor's angiogenesis. This is probably one of the most important mechnisms of inhibiting glioma.
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