普朗克127修饰氧化石墨烯载盐酸阿霉素抗人神经胶质瘤的机制研究

发布时间：2018-03-12 18:46

本文选题：盐酸阿霉素　切入点：氧化石墨烯　出处：《吉林大学》2017年硕士论文　论文类型：学位论文

【摘要】：目的:研究、探讨PF127-GO-DOX抗人神经胶质瘤的作用及其相关分子机制,为肿瘤的信号通路分子靶向治疗提供更多的证据。方法:(1)培养人源性胶质瘤细胞系U251细胞:U251细胞的复苏、培养与冻存;(2)比较PG、PF127-GO、DOX、PF127-GO对U251细胞凋亡的作用:实验分为4组:模型组、PF127-GO组、DOX组、PF127-GO-DOX组,流式细胞仪检测细胞凋亡率;(3)提取U251细胞株胞浆蛋白,Western-blotting法测定P53、细胞外信号调节蛋白激酶1/2(extracellular signal-regulated kinases 1/2,ERK1/2),c-jun氨基末端激酶/(c-Jun amino(N)-terminal kinases,JNK)、半胱氨酸的天冬氨酸蛋白水解酶-3(cysteinyl aspartate specific proteinase,Caspase-3)的表达水平。结果:(1)PF127-GO-DOX、DOX对胶质瘤U251细胞有明显的促凋亡作用;(2)PF127-GO-DOX可以上调P53、JNK、Caspase-3,下调ERK1/2的表达。结论:(1)PF127-GO-DOX对人胶质瘤细胞有较强的促凋亡作用,且优于单独的DOX;(2)PF127-GO-DOX可能通过激活JNK及P53通路,抑制ERK1/2通路,诱导肿瘤细胞凋亡,发挥抗胶质瘤作用。
[Abstract]:Objective: to investigate the effect of PF127-GO-DOX on human glioma and its related molecular mechanism, and to provide more evidence for the molecular targeting therapy of tumor signaling pathway. Methods: human glioma cell line U251 cell line: U251 cell line was resuscitated. The effect of PGN PF127-GOXP127-GO on apoptosis of U251 cells was compared. The experiment was divided into four groups: model group, PF127-go group, DOX group, PF127-GO-DOX group. Extracellular signal regulated protein kinase 1 / 2 extracellular signal-regulated kinases 1 / 2 ERK1 / 2 ERK1 / 2 ERK1 / 2ERK-1 / 2ERK-1 / 2ERK-1 / 2ERK-1 / 2ERK-1 / 2, c-Jun amino(N)-terminal kinaseshs / JNKK, cysteine aspartyl aspartate specific proteinase / caspase-3 (Caspase-3), cytoplasmic protein hydrolase (-3cysteinyl aspartate specific proteinase) of U251 cell line (U251 cell line) was extracted by flow cytometry (FCM) and extracellular signal regulated protein kinase (extracellular signal-regulated / kinases 1 / 2 / 2 / 2 / 2 / 2). Results PF127-GO-DOX could significantly promote apoptosis in U251 glioma cells and could up-regulate the expression of P53, JNK-Caspase-3 and down-regulate the expression of ERK1/2. Conclusion: F127-GO-DOX has a strong apoptotic effect on human glioma cells. In addition, PF127-GO-DOX may inhibit ERK1/2 pathway, induce apoptosis of tumor cells and play an anti-glioma role by activating JNK and p53 pathway.
【学位授予单位】：吉林大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R739.41

【相似文献】