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目的:探究新霉素、苯丁酸钠及两者联合应用对胶质瘤抑制作用的机制。方法:F98胶质瘤细胞注入Fischer344大鼠尾状核头制成胶质瘤模型。于种植后第10天将新霉素10 mmol·L-1作为局部用药注入到肿瘤中心,苯丁酸钠全身用药。分别于治疗后第6、12、18天MRI增强扫描计算肿瘤体积;18 d后用免疫组化技术对肿瘤标本的C-myc、Cyclin D1、第Ⅷ和TUNEL进行标记染色观察药物抑制。结果:治疗组60只鼠全部存活,对照组10只中有8只死亡;与对照组相比,所有治疗组标本中的C-myc和Cyclin D1蛋白染色计数均有显著减少(P<0.05),凋亡细胞数显著增多(P<0.01)。其中新霉素治疗组血管计数显著减少(P<0.01);苯丁酸钠组前后对比血管计数没有变化(P>0.05)。结论:新霉素和苯丁酸钠单用后对胶质瘤生长均有抑制作用,联合用药后效果更明显。机制可能是同时下调C-myc和Cyclin D1基因的表达,抑制肿瘤细胞的增殖,诱导凋亡。新霉素还阻止肿瘤血管的形成,遏制了肿瘤。
Objective: To explore the mechanism of neomycin, sodium phenylbutyrate and the combination of both of them on glioma inhibition. METHODS: F98 glioma cells were injected into caudate nucleus of Fischer344 rat to make a glioma model. On the 10th day after planting, neomycin 10 mmol·L-1 was injected into the tumor center as a topical drug, and sodium phenylbutyrate was administered systemically. The volume of tumor was calculated by MRI enhanced scanning on the 6th, 12th and 18th day after treatment respectively. On the 18th day, C-myc, Cyclin D1, Ⅷ and TUNEL were stained by immunohistochemistry to observe the drug inhibition. Results: All the 60 mice survived in the treatment group, and 8 of 10 mice died in the control group. Compared with the control group, the staining counts of C-myc and Cyclin D1 were significantly decreased in all treatment groups (P <0.05) , The number of apoptotic cells increased significantly (P <0.01). Among them, the neovascularization group had a significant decrease in the number of vessels (P <0.01), but no significant change in the blood counts before and after sodium phenylbutyrate treatment (P> 0.05). CONCLUSION: Both neomycin and sodium phenylbutyrate can inhibit the growth of glioma alone, and the effect is more obvious when combined with neomycin and sodium phenylbutyrate. Mechanism may be down-regulation of C-myc and Cyclin D1 gene expression, inhibition of tumor cell proliferation, induce apoptosis. Neomycin also prevents the formation of tumor blood vessels, containing the tumor.