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东亚钳蝎神经毒素(BmK CT)能特异性地阻断神经胶质瘤细胞的氯离子通道,抑制胶质瘤细胞的侵袭力。本文旨在研究125I-BmK CT对大鼠胶质瘤细胞(C6)侵袭的影响及作用机制。采用transwell小室评价125I-BmK CT对C6细胞侵袭能力的影响,采用酶联免疫吸附试验(ELISA法)、实时荧光定量聚合酶链反应(Real-Time PCR)和Western-Blot检测125I-BmK CT对C6的基质金属蛋白酶-2(MMP2)基因和蛋白表达水平的影响。实验结果表明,125I-BmK CT可显著抑制C6细胞的侵袭能力(P<0.05);显著抑制C6细胞分泌MMP2(P<0.05);C6细胞经125I-BmK CT处理后,MMP2的mRNA表达未见明显变化,差异无统计学意义(P>0.05),MMP2的蛋白合成被显著抑制(P<0.05)。研究结果证明,125I-BmK CT可显著抑制C6细胞的侵袭能力,其机制可能与MMP2的分泌和蛋白合成水平降低有关。
Bcl-2 neurotoxin (BmK CT) can specifically block the chloride channel of glioma cells and inhibit the invasiveness of glioma cells. The aim of this study was to investigate the effects of 125I-BmK CT on invasion of rat glioma cells (C6) and its mechanism. The effect of 125I-BmK CT on invasiveness of C6 cells was evaluated by transwell chamber. The 125I-BmK CT was detected by enzyme-linked immunosorbent assay (ELISA), Real-time PCR and Western-Blot C6 matrix metalloproteinase -2 (MMP2) gene and protein expression levels. The results showed that 125I-BmK CT could significantly inhibit the invasion of C6 cells (P <0.05), inhibit the secretion of MMP2 significantly (P <0.05), and the expression of MMP2 mRNA in C6 cells treated with 125I-BmK CT (P> 0.05). The protein synthesis of MMP2 was significantly inhibited (P <0.05). The results show that 125I-BmK CT can significantly inhibit the invasion of C6 cells, the mechanism may be related to the secretion of MMP2 and reduced protein synthesis level.