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目的针对人小脑血管母细胞瘤(hemangioblastoma,HB)中缺氧诱导因子1α(hypoxia induciblefactor-1α,HIF-1α)和血管内皮生长因子(vascular endothelial growth factor,VEGF)的表达情况,探讨其具体调控机制和在HB发生发展中的作用。方法采用逆转录聚合酶链反应(reverse transcription polymerase chain reaction,RT-PCR)和免疫组织化学法分别检测5例新鲜冷冻标本及30例多聚甲醛固定的人小脑HB标本中HIF-1α与VEGF的表达情况,并对实验结果进行半定量计算和统计学分析。结果 RT-PCR结果示正常小脑和HB组织中HIF-1α与内参GAPDH的mRNA平均光密度值比值分别为0.036±0.005和0.578±0.134;VEGF与内参GAPDH的mRNA平均光密度值比值分别为0.039±0.008和0.676±0.238;2组间差异均有统计学意义(P<0.05)。免疫组织化学结果显示HIF-1α在正常小脑和HB组织中的阳性表达率分别为10.0%和93.3%,VEGF的阳性表达率分别为10.0%和96.6%;2组间差异均有统计学意义(P<0.01)。结论 HIF-1α与VEGF在人小脑HB中无论是在mRNA水平还是在蛋白水平均为高表达,并且2者间的表达具有相关性;人小脑HB中HIF-1α与VEGF的上调有别于其他肿瘤组织中以缺氧为始动因素的调控方式。
Objective To investigate the expression of hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) in human cerebellar hemangioblastoma (HB) Mechanism and role in the occurrence and development of HB. Methods Reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry were used to detect the expression of HIF-1α and VEGF in 5 fresh frozen samples and 30 paraformaldehyde fixed human cerebellum HB samples respectively. Expression, and the experimental results were semi-quantitative and statistical analysis. Results RT-PCR results showed that the average OD value of HIF-1α and GAPDH in normal cerebellum and HB tissues were 0.036 ± 0.005 and 0.578 ± 0.134, respectively. The average OD value of VEGF and GAPDH were 0.039 ± 0.008 and 0.676 ± 0.238, respectively. There was significant difference between the two groups (P <0.05). The results of immunohistochemistry showed that the positive rates of HIF-1α in normal cerebellum and HB were 10.0% and 93.3% respectively, and the positive rates of VEGF were 10.0% and 96.6% respectively. There was significant difference between the two groups P <0.01). Conclusions HIF-1α and VEGF are highly expressed in human cerebellum HB both in mRNA and protein level, and the expression of HIF-1α and VEGF is correlated. The up-regulation of HIF-1α and VEGF in human cerebellum HB is different from other Hypoxia as a motivating factor in the regulation of tumor tissue.