中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2009年
25期
1736-1740
,共5页
李兴起%张胜华%欧阳志钢%甄永苏
李興起%張勝華%歐暘誌鋼%甄永囌
리흥기%장성화%구양지강%견영소
细胞,胶质瘤%细胞凋亡,诱导%新生血管化,病理性%力达霉素
細胞,膠質瘤%細胞凋亡,誘導%新生血管化,病理性%力達黴素
세포,효질류%세포조망,유도%신생혈관화,병이성%력체매소
Cells,glioma%Apoptosis,induction%Neovascularization,pathologic%Lidamycin
目的 评价烯二炔类抗生素力达霉素对神经胶质瘤细胞血管生成拟态的抑制作用及对细胞凋亡的影响.方法 C6和U87细胞凋亡以Annexin V-FITC/PI法结合流式细胞仪法进行分析,小管形成实验分析药物对神经胶质瘤细胞血管拟态的影响.结果 0.1 nmol/L(12.7±0.6)、0.5nmol/L(9.0±1.7)和1 nmol/L(4.7±0.6)力达霉素处理的C6细胞血管生成拟态与对照(16.7±1.5)相比,差异有统计学意义(分别为P=0.013、P=0.005及P=0.0002);同样浓度的药物对U87细胞的血管生成拟态与对照(14.7±1.2)相比,差异有统计学意义(分别为P=0.025、P=0.005及P=0.0009).相同剂量的力达霉素处理C6和U87细胞后其凋亡率与相应对照组相比差异有统计学意义.力达霉素对神经胶质瘤细胞血管生成拟态和细胞凋亡的影响明显比新制癌菌素强.结论 力达霉素能够抑制神经胶质瘤细胞血管生成拟态并促进神经胶质瘤细胞凋亡,烯二炔类抗肿瘤抗生素治疗神经胶质瘤的研究值得进一步探讨.
目的 評價烯二炔類抗生素力達黴素對神經膠質瘤細胞血管生成擬態的抑製作用及對細胞凋亡的影響.方法 C6和U87細胞凋亡以Annexin V-FITC/PI法結閤流式細胞儀法進行分析,小管形成實驗分析藥物對神經膠質瘤細胞血管擬態的影響.結果 0.1 nmol/L(12.7±0.6)、0.5nmol/L(9.0±1.7)和1 nmol/L(4.7±0.6)力達黴素處理的C6細胞血管生成擬態與對照(16.7±1.5)相比,差異有統計學意義(分彆為P=0.013、P=0.005及P=0.0002);同樣濃度的藥物對U87細胞的血管生成擬態與對照(14.7±1.2)相比,差異有統計學意義(分彆為P=0.025、P=0.005及P=0.0009).相同劑量的力達黴素處理C6和U87細胞後其凋亡率與相應對照組相比差異有統計學意義.力達黴素對神經膠質瘤細胞血管生成擬態和細胞凋亡的影響明顯比新製癌菌素彊.結論 力達黴素能夠抑製神經膠質瘤細胞血管生成擬態併促進神經膠質瘤細胞凋亡,烯二炔類抗腫瘤抗生素治療神經膠質瘤的研究值得進一步探討.
목적 평개희이결류항생소력체매소대신경효질류세포혈관생성의태적억제작용급대세포조망적영향.방법 C6화U87세포조망이Annexin V-FITC/PI법결합류식세포의법진행분석,소관형성실험분석약물대신경효질류세포혈관의태적영향.결과 0.1 nmol/L(12.7±0.6)、0.5nmol/L(9.0±1.7)화1 nmol/L(4.7±0.6)력체매소처리적C6세포혈관생성의태여대조(16.7±1.5)상비,차이유통계학의의(분별위P=0.013、P=0.005급P=0.0002);동양농도적약물대U87세포적혈관생성의태여대조(14.7±1.2)상비,차이유통계학의의(분별위P=0.025、P=0.005급P=0.0009).상동제량적력체매소처리C6화U87세포후기조망솔여상응대조조상비차이유통계학의의.력체매소대신경효질류세포혈관생성의태화세포조망적영향명현비신제암균소강.결론 력체매소능구억제신경효질류세포혈관생성의태병촉진신경효질류세포조망,희이결류항종류항생소치료신경효질류적연구치득진일보탐토.
Objective To evaluate the in vitro effects of lidamycin upon vasculogenic mimicry and apoptosis induction in glioma cells. Methods Tube formation assay was performed to estimate the inhibitory effects of lidamycin upon vasculogenic mimicry in C6 and U87 glioma cells. The vasculogenic mimicry of glioma cells was photographed and enumerated. Annexin V-FITC/PI was used for determination of glioma cell apoptosis with flow cytometry. Results Vasculogenic mimicry assay indicated that 0. 1 nmol/L, 0. 5 nmol/L and 1 nmol/L lidamycin showed significant inhibition of vasculogenic mimicry in C6 and U87 cells. Comparing with C6 control group (14. 7 ± 1.2), 0. 1 nmol/L (12. 7 ± 0. 6), 0. 5 nmol/L (9. 0 ± 1.7) and 1 nmol/L (4. 7 ± 0. 6) lidamycin inhibited vasculogenic mimicry in C6 cells with statistical significances (P = 0. 013, P = 0. 005 and P = 0. 0002 respectively). Comparing with U87 control group (14.7±1.2), the vasculogenic mimicry of 0.1 nmol/L (10.0±2.0), 0.5 nmol/L (8.3±1.5) and 1 nmol/L lidamycin (4. 3±0. 6) treated U87 cells showed statistical significances (P =0. 025, P =0. 005 and P =0. 0009 respectively). The apoptotic ratios of same dosages lidamycin treated C6 cells and U87 cells showed a similar tendency as vaaculogenic mimicry inhibition (P < 0. 001). Lidamycin was more potent than neocarzinostatin in vasculogenic mimicry inhibition and apoptosis induction of C6 cells and U87 cells. Conclusion Lidamycin can inhibit vasculogenic mimicry and promote apotosis of glioma cells. Thus it is a promising drug in glioma treatment. Further researches on the therapeutic efficacy of enediyne antibiotics in glioma are needed.