Inhibitory effects of lapachol on rat C6 glioma in vitro and in vivo by targeting DNA topoisomerase Ⅰ and topoisomerase Ⅱ

OBJECTIVE The aim of this study is to investigate the inhibitory effects of lapachol on rat C6 glioma both in vitro and in vivo,as well as the potential mechanisms.METHODS First,the model of C6 glioma in Wistar rats was established and verified by hemotoxylin and eosin staining,immunohistochemical staining and magnetic resonance imaging(MRI).Then different doses of lapachol were gavaged and tumor volumes of the C6 glioma were detected by MRI.The effects of lapachol on C6 cell proliferation,apoptosis and DNA damage were detected by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium(MTS)/phen-azinemethosulfate(PMS)assay,Hoechst33358 staining,AnnexinⅤ-FITC/PI staining,and comet assay.Effects of lapachol on topoisomeraseⅠ(TOPⅠ)and topoisomeraseⅡ(TOPⅡ)activities were detected by TOPⅠand TOPⅡmediated supercoiled p BR322 DNA relaxation assay.Molecular docking was used to predict the interaction of lapachol-TOPⅠand lapachol-TOPⅡ.TOP I and TOPⅡexpression levels in C6 cells were determined by Enzymelinked immunosorbent assay kits and real-time polymerase chain reaction(RT-PCR).RESULTS The rat C6 glioma model was successfully established.High dose lapachol showed significant inhibitory effect on the C6 glioma in Wistar rats(P<0.05).MTS/PMS assay,Hoechst 33258 staining,AnnexinⅤ-FITC/PI staining,and comet assay showed that lapachol could inhibit proliferation,induce apoptosis and DNA damage of C6 cells in dose dependent manners.Lapachol could inhibit the activities of both TOPⅠandⅡ.Molecular docking showed that lapachol-TOPⅠshowed relatively stronger interaction than that of lapachol-TOPⅡ.Enzyme-linked immunosorbent assay and RT-PCR showed that lapachol could inhibit TOPⅡexpression levels,but not TOPⅠexpression levels.CONCLUSION These results showed that lapachol could significantly inhibit C6 glioma both in vivo and in vitro,which might be related with inhibiting TOPⅠand TOPⅡactivities,as wel as TOPⅡexpression.

Inhibitory effects of lapachol on rat C6 glioma in vitro and in vivo by targeting DNA topoisomeraseⅠ and topoisomeraseⅡ

OBJECTIVE Lapachol is a natural naphthoquinone compound that possesses extensive biological activities.The aim of this study is to investigate the inhibitory effects of lapachol on rat C6 glioma both in vitro and in vivo,as well as the potential mechanisms.METHODS The antitumor effect of lapachol was firstly evaluated in the C6 glioma model in Wistar rats.The effects of lapachol on C6 cell proliferation,apoptosis and DNA damage were detected by 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium(MTS)/phenazinemethosulfate(PMS)assay,hoechst 33358 staining,annexinⅤ-FITC/PI staining,and comet assay.Effects of lapachol on topoisomerase I(TOP I)and topoisomeraseⅡ(TOPⅡ)activities were detected by TOPⅠand TOPⅡmediated supercoiled p BR322DNA relaxation assays and molecular docking.TOPⅠand TOPⅡexpression levels in C6 cells were also determined.RESULTS High dose lapachol showed significant inhibitory effect on the C6 glioma in Wistar rats(P<0.05).It was showed that lapachol could inhibit proliferation,induce apoptosis and DNA damage of C6 cel s in dose dependent manners.Lapachol could inhibit the activities of both TOPⅠ and Ⅱ.Lapachol-TOPⅠshowed relatively stronger interaction than that of lapachol-TOPⅡin molecular docking study.Also,lapachol could inhibit TOPⅡexpression levels,but not TOPⅠexpression levels.CONCLUSION These results showed that lapachol could significantly inhibit C6 glioma both in vivo and in vitro,which might be related with inhibiting TOPⅠ and TOPⅡ activities,as wel as TOPⅡ expression.

Ki-67及TopoisomeraseⅡ在脑胶质母细胞瘤组织中的表达及其生物学意义

目的探讨人胶质母细胞瘤中Ki-67及TopoisomeraseⅡ（TopoⅡ）之间的相关性及其与胶质母细胞瘤病人预后的关系。方法收集O6-甲基鸟嘌呤-DNA甲基转移酶（MGMT）低表达的胶质母细胞瘤标本60例,应用免疫组化法检测Ki-67和TopoⅡ的表达,研究其相关性。结果在MGMT低表达的胶质母细胞瘤中,Ki-67与TopoⅡ表达呈正相关（γ=0.83,P〈0.05）。对本组标本来源的60例胶质母细胞瘤病人随访12~23个月,其中死亡38例,肿瘤复发46例。结论 Ki-67和TopoⅡ在胶质母细胞瘤中的表达强度相对一致;其表达能客观反映肿瘤细胞的增殖活性和恶性程度,且可能影响胶质母细胞瘤病人的预后。

免疫组化检测大肠癌GST-π、TopoisomeraseⅡ-α表达的临床意义

目的 探讨GST -π、TopoisomeraseⅡ -α蛋白与大肠癌病理学特征之间的关系。方法 分别用鼠抗人TopoisomeraseⅡ -α单克隆抗体和兔抗人GST -π抗体对 6 0例大肠癌石蜡标本进行免疫组化研究。结果 1.GST -π、TopoisomeraseⅡ -α蛋白的表达和肿瘤大小、部位及类型无关 (P >0 .0 5 ) ;但与肿瘤的分化程度、临床分期、淋巴结转移有统计学差异 (P <0 .0 0 1)。 2 .GST -π在癌灶及癌旁组织中的表达意义不同 ,在肿瘤组织中低分化组高表达而在癌旁组织中则低表达 ,二者有统计学差异 (P <0 .0 0 1) ;TopoisomeraseⅡ -α在高分化组的表达高于低分化组 (P <0 .0 0 1)。结论 1.GST -π在瘤组织中的表达强度及在癌旁组织中的表达均与肿瘤的分化及临床分期有关 ,可作为肿瘤预后的指标。 2 .Topoi someraseⅡ -α在肿瘤组织中的表达和其分化、淋巴结转移有关 。

TopoisomeraseⅡ-α在大肠癌中的表达和临床意义

目的 探讨TopoisomeraseⅡ α蛋白与大肠癌病理学特征之间 ,耐药之间的关系。 方法 分别用鼠抗人TopoisomeraseⅡ α单克隆抗体对 60例大肠癌石蜡标本进行免疫组化研究。 结果 TopoisomeraseⅡ α蛋白及癌旁组织中的表达和性别、肿瘤大小、部位及类型无关 (P >0 .0 5 ) ;但与肿瘤的分化程度、Dukes分期、TMN分期、临床分期、淋巴结转移有统计学差异 (P <0 .0 0 1)。TopoisomeraseⅡ α在高分化组的表达高于低分化组 (P <0 .0 0 1) ,淋巴结转移组表达则低于无淋巴结转移组 (p <0 .0 0 1)。结论 TopoisomeraseⅡ α在肿瘤组织中的表达 ,强度和肠癌生物学特性密切相关 ,与肿瘤的分化及临床分期、淋巴结转移有关 ,可做为衡量恶性程度 ,耐药性及预后的指标之一。

共刺激分子B7H3通过调控DNA拓扑异构酶Ⅱα的表达对乳腺癌多柔比星化疗的影响

目的探讨共刺激分子B7H3(costimulatory molecule B7H3,B7H3)通过调控DNA拓扑异构酶Ⅱα(DNA topoisom eraseⅡalpha,TOP2A)的表达对乳腺癌多柔比星化疗敏感性的影响。方法收集临床标本,采用免疫组织化学染色验证B7H3表达与多柔比星化疗敏感性的相关性。采用成簇规律间隔短回文重复/Cas9基因编辑技术敲除B7H3,通过蛋白质印迹法和流式细胞术验证敲除结果。采用半抑制浓度值分析、集落形成、蛋白质印迹法检测凋亡蛋白、荧光双染色检测凋亡细胞以及细胞周期测定等方法验证B7H3表达与多柔比星作用的敏感性。小干扰TOP2A及其过表达TOP2A回复实验检测细胞凋亡。构建小鼠皮下成瘤模型验证体内B7H3表达与多柔比星化疗的作用。结果高表达B7H3的肿瘤组织对多柔比星治疗更加敏感。成功构建B7H3敲除的乳腺癌细胞。B7H3高表达的乳腺癌细胞对多柔比星作用更敏感。B7H3通过激活核因子κB(nuclear factor-κB,NF-κB)途径促进TOP2A的表达,进而增加乳腺癌细胞对多柔比星作用的敏感性。小鼠体内实验证明,B7H3高表达可增加乳腺癌对多柔比星化疗的敏感性。结论B7H3通过激活NF-κB通路调控TOP2A的表达使乳腺癌对多柔比星化疗更敏感。

THE ANTICANCER EFFECT AND ANTI－DNA TOPOISOMERASE II EFFECT OF EXTRACTS OF CAMELLIA PTILOPHYLLA CHANG AND CAMELLIA SINENSIS

The cytotoxic effect of extract of camellia ptilophyllachang(ECPC) and extract of camellia sinensis(ECS) onHeLa cell line, poorly differentiated nasopharyngealcarcinoma cell line(CNE2) and gastric cancer cell line(MGC-803 ) in vitro was studied using MIT assay method.The results showed that ECPC and ECS possessed significantcytotoxic effect on above three cell lines. The anticancer testin mice showed that ECPC had marked inhibitory effectagainst Ehrlich solid carcinoma(ESC) with inhibition ratesof 17. 8 48. 3% and with inhibition rates of 28. 3-54. 5% against reticular cell sarcoma(L2), and that ECShad inhibition rates of 31 . 5 -49. 4 % against ESC and 35. 8- 50% against L2. These two extracts had only marginalinhibitory effect against sarcoma- 180. The unknottingactivity of DNA topoisomerase II was inhibited completelyby ECPC and ECS at the concentration of 50 μg/ mlsuggesting that DNA topoisomerase II might be a targetenzyme of these two extracts.

EFFECT OF ACTIVE COMPOUNDS ISOLATED FROM PTERIS SEMIPINNATA L ON DNA TOPOISOMERASES AND TYROSINE PROTEIN KINASE AND EXPRESSION OF C-MYC IN LUNG ADENOCARCINOMA CELLS

Objective: To study the effect of active compound 6F and A from Pteris semipinnata L.(PsL) on the activities of DNA topoisomerase (TOPO) I and II, activities of cytosolic and membrane TPK, and expression of oncogene c-myc in lung adenocarcinoma cells. Methods: The effect of compound 6F and A on activities of cytosolic and membrane TPK was measured by scintillation counting; the effect of compound A on expression of oncogene c-myc was determined by flow cytometry indirect fluorimetry. Results: compound 6F and A could inhibit the activities of TOPO I, and they strongly inhibited the TOPO II in 0.01 mg/L and 10.0 mg/L respectively. Compound A slightly inhibited the activities of membrane TPK, but not the cytosolic one. Compound A could inhibit the expression of oncogene c-myc. Conclusion: Topoisomerases are target of compound 6F and A. Compound A could slightly inhibit the activities of TPK, and showed an inhibitory effect on the expression of oncogene c-myc.

TopoisomeraseⅡαGene as a Marker for Prognostic Prediction of Hepatocellular Carcinoma:A Bioinformatics Analysis

Objective To investigate the expression of topoisomeraseⅡα(TOP2α)in hepatocellular carcinoma(HCC)and its role in predicting prognosis of HCC patients.Methods We used HCC-related datasets in UALCAN,HCCDB,and cBioPortal databases to analyze the expression and mutation of TOP2αand its co-expressed genes in HCC tissues.GO function and KEGG pathway enrichment of TOP2αand its co-expressed genes were identified.The TIMER database was used to analyze infiltration levels of immune cells in HCC.The impacts of TOP2αand its co-expression genes and the infiltrated immune cells on the survival of HCC patients were assayed by Kaplan-Meier plotter analysis.Results TOP2αand its co-expression genes were highly expressed in HCC(P<0.001)and detrimental to overall survival of HCC patients(P<0.001).TOP2αand its co-expression genes were mainly involved in cell mitosis and proliferation,and cell cycle pathway(ID:hsa04110,P=0.001945).TOP2αand its co-expression genes were mutated in HCC and the mutations were significantly detrimental to overall survival(P=0.0247)and disease-free survival(P=0.0265)of HCC patients.High TOP2αexpression was positively correlated with the infiltration of B cell(r=0.459,P<0.01),CD8^(+)T cell(r=0.312,P<0.01),CD4^(+)T cell(r=0.370,P<0.01),macrophage(r=0.459,P<0.01),neutrophil(r=0.405,P<0.01),and dendritic cell(r=0.473,P<0.01)in HCC.The CD8^(+)T cell infiltration significantly prolonged the 3-and 5-year survival of HCC patients(all P<0.05),and CD4^(+)T cell infiltration significantly shortened the 3-,5-,and 10-year survival of HCC patients(all P<0.05).Conclusion TOP2αmay be an oncogene,which was associated with poor prognosis of HCC patients and could be used as a biomarker for the prognostic prediction of HCC.

纳米塑料诱导肺泡Ⅱ型上皮细胞DNA损伤加重重症哮喘

目的·探讨纳米塑料(nanoplastics,NPs)对重症哮喘发生发展的影响及潜在分子机制。方法·建立屋尘螨(house dust mite,HDM)和脂多糖(lipopolysaccharide,LPS)联合诱导的重症哮喘小鼠模型,并给予聚苯乙烯纳米塑料(polystyrene nanoplastics,PS-NPs)气道滴注,收集小鼠肺泡灌洗液及制作肺组织切片。通过流式细胞术、苏木精-伊红(hematoxylin-eosin,H-E)染色、过碘酸希夫(periodic acid-Schiff,PAS)染色、免疫组织化学染色、脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(terminal dexynucleotidyl transferase-mediated dUTP nick-end labeling,TUNEL)染色,观察PS-NPs对重症哮喘小鼠气道炎症、黏液分泌、肺泡结构,以及肺泡Ⅱ型上皮细胞(alveolar typeⅡepithelial cells,AT2 cells)增殖和凋亡的影响。采用CCK-8法及AnnexinⅤ/PI双染色法测定PS-NPs对小鼠AT2细胞系MLE-12细胞增殖、凋亡的影响。使用γ-H2A.X免疫荧光染色检测PS-NPs对AT2细胞的DNA损伤作用。通过实时荧光定量聚合酶链反应(realtime fluorescent quantitative polymerase chain reaction,qPCR)、蛋白质印迹法(Western blotting)、酪胺信号放大(Tyramide signal amplification,TSA)多重荧光染色及免疫荧光共定位检测PS-NPs对AT2细胞ATR/Chk1/p53信号通路相关基因和蛋白表达的影响。使用ATR特异抑制剂Ceralasertib(AZD6738)与PS-NPs共同处理MLE-12细胞,以测定其对细胞增殖、凋亡的恢复作用。结果·流式细胞术显示,重症哮喘小鼠暴露于PS-NPs后,其肺泡灌洗液中炎症细胞总数及各炎症细胞数量均有增加,以中性粒细胞增多为主;肺组织H-E染色及PAS染色显示,气道炎症细胞浸润及气道黏液分泌显著增加,肺泡结构被破坏。在体外试验中,CCK-8结果显示PS-NPs显著抑制MLE-12细胞的增殖能力并呈现浓度依赖性;AnnexinⅤ/PI双染色结果显示,PS-NPs暴露后的细胞凋亡率[(56.20±3.84)%]相比于未暴露组[(23.22±2.52)%]显著上升;免疫荧光染色显示PS-NPs能被MLE-12细胞所吞噬并定位在细胞核周围。TUNEL染色结果表明,在体内PS-NPs同样促进AT2细胞凋亡的发生。免疫荧光染色结果显示,与对照组相比,实验组DNA损伤标志物γ-H2A.X表达增加。qPCR、Western blotting、TSA多重荧光染色显示,PS-NPs诱导MLE-12细胞ATR/Chk1/p53信号通路相关基因和蛋白表达水平升高。免疫荧光共定位实验也证实在小鼠体内,PS-NPs诱导AT2细胞表达ATR、p53蛋白。而ATR特异抑制剂Ceralasertib能部分恢复由PS-NPs引起的MLE-12细胞增殖的抑制和凋亡的增强。结论·NPs暴露能够造成AT2细胞DNA损伤,激活ATR/Chk1/p53信号通路,进而加重重症哮喘小鼠气道炎症反应及肺泡结构损伤。

血清PIVKA-Ⅱ、AFP与HBV-DNA联合检测对HBV所致肝癌的诊断及预后预测价值

目的探究血清异常凝血酶原Ⅱ(PIVKA-Ⅱ)、甲胎蛋白(AFP)与乙肝病毒脱氧核糖核酸(HBV-DNA)联合检测对HBV所致肝癌(HCC)的诊断及预后预测价值。方法选取2018年8月至2020年7月在本院接受治疗的98例HCC患者作为研究对象(肝癌组),另取同期95例体检健康人群作为健康组,95例肝硬化患者作为肝硬化组,观察3组受试者血清PIVKA-Ⅱ、AFP与HBV-DNA表达水平和一般资料差异。根据肝癌组3年内预后情况将患者分为生存组(57例)和死亡组(41例)。比较肝癌组一般资料和血清PIVKA-Ⅱ、AFP与HBV-DNA水平关系;多因素Logistic和COX回归分析分别分析影响受试者患肝癌和患者预后不良的影响因素;四格表法计算血清PIVKA-Ⅱ、AFP与HBV-DNA水平对HCC的预测价值;ROC曲线分析评估血清PIVKA-Ⅱ、AFP与HBV-DNA水平对HCC患者预后的预测价值。结果肝癌组患者血清PIVKA-Ⅱ、AFP与HBV-DNA水平显著高于健康组和肝硬化组(P<0.05);HCC发病与血清PIVKA-Ⅱ、AFP与HBV-DNA水平有关,且是危险因素(P<0.05)。HCC患者预后不良与血清PIVKA-Ⅱ、AFP与HBV-DNA水平以及肿瘤数量有关(P<0.05),且是危险因素。血清PIVKA-Ⅱ、AFP与HBV-DNA水平以及3项联合诊断HCC发病的准确度分别为77.43%、72.57%、77.43%和84.72%。血清PIVKA-Ⅱ、AFP与HBV-DNA水平以及3项联合诊断HCC预后不良的AUC分别为0.823、0.841、0.824和0.958,3项联合诊断效能优于单一诊断(P<0.05)。结论血清PIVKA-Ⅱ、AFP与HBV-DNA水平在HCC患者和预后不良患者中呈高表达,且3项联合可有效预测HCC发病和HCC患者预后情况。

EFFECT OF ANTITUMOR DRUGS ON THE ACTIVITY OF DNA TOPOISOMERASE I

The activity of DNA topoisomerase Ⅱ prepared from either normal or tumor tissues were compared. It was found that the unknotting activity of the enzyme in malignant tumor cells was higher than that in normal cells. We selected some antitumor drugs including Chinese traditional medicine, and observed their effects on the unknotting activity of topoisomerase Ⅱ. The results showed that inhibition of the unknotting activity of the enzyme required very low concentrations of drugs, but much higher concentrations were required for other tested. Some antitumor drugs had no effect on the enzyme were also proved. It is interesting that carrageenan, an antiviral drug, strongly blocked the unknotting activity although its antitumor activity has not been reported.

骆驼蓬种子提取物及其β咔保啉生物碱对DNA拓扑异构酶Ⅱ活性的抑制作用

目的探讨去氢骆驼蓬碱、骆驼蓬碱、骆驼蓬总碱及哈尔满碱(止咳药用植物)对DNA拓扑异构酶Ⅱ活性的抑制作用。方法从体外培养的Q3肝癌细胞中,提取分离DNA拓扑异构酶Ⅱ;以阿霉素为阳性对照,用琼脂糖凝胶电泳法检测药物对DNA拓扑异构酶Ⅱ的作用。结果骆驼蓬总碱、去氢骆驼蓬碱、骆驼蓬碱及哈尔满碱对DNA拓扑异构酶Ⅱ活性均有一定的抑制作用。结论对DNA拓扑异构酶Ⅱ活性的抑制作用是骆驼蓬总碱、去氢骆驼蓬碱、骆驼蓬碱等生物碱抗癌作用和细胞毒作用的机制之一。

铜(Ⅱ)邻菲咯啉蛋氨酸配合物与DNA相互作用的研究

在pH =6 86磷酸盐缓冲溶液中 ,采用电化学 (循环伏安法、微分脉冲伏安法和交流阻抗及数据拟合技术 )、粘度测定、电子吸收光谱和溴化乙锭 (EB)荧光分析法研究了 [Cu(phen) (H2 O) (L Met) ] + (phen =1,10 邻菲咯啉 ,L Met =L 蛋氨酸 )与小牛胸腺DNA的相互作用 .结果发现中心铜离子在循环伏安图上呈现 1对明显的准可逆氧化还原波 .当加入一定量的DNA时 ,配合物的氧化还原峰电流明显降低 ,扩散系数减小 ,电化学反应电阻增大 ,电子光谱的最大吸收峰明显红移 ,产生明显的减色效应 ,同时 ,配合物也能较大程度地猝灭EB DNA体系的荧光 ,说明 [Cu(phen) (H2 O) (L Met) ] + 与DNA的作用较强 。

中国境内不同地理型东方蜜蜂线粒体DNA tRNA^(leu)～COⅡ基因多态性研究

【目的】从线粒体水平上探讨中国境内不同地理型东方蜜蜂的系统发育关系,为东方蜜蜂亚种分化的研究及我国境内东方蜜蜂资源的保护与合理开发利用提供基础资料。【方法】采用公开的E2、H2引物对11个不同地理型东方蜜蜂线粒体DNA tRNAleu～COⅡ基因进行了PCR扩增、测序,并利用相关软件和网站进行了序列比较分析。【结果】该序列长度为471bp;序列中共有9个位点发生变异;序列相似性均在99%以上;限制性酶切分析表明:云南保山东方蜜蜂缺少一个SwaⅠ酶切位点;部分编码蛋白序列比对表明,海南海口和吉林安图东方蜜蜂各有一个氨基酸发生变异。与GeneBank上公开登录的国内外有关东方蜜蜂相关序列的比较表明,单纯利用非编码区序列对比,不能把日本蜜蜂同中国大陆的东方蜜蜂区别开来;COⅡ基因部分序列对比显示,东方蜜蜂的线粒体类型包括:日本-韩国型、中国大陆型、中国台湾型、马来西亚沙巴州-印度黑色蜜蜂型、中国海南型、印度黄色蜜蜂型、泰国南部型和印度黑色蜜蜂型。【结论】中国境内不同地理型东方蜜蜂存在着较明显的遗传分化,其中海南东方蜜蜂由于长期的海岛隔离形成了一个独特的类群,支持了通过形态学认定的海南东方蜜蜂为东方蜜蜂的一个新亚种的观点。本研究部分测序结果已在美国国家生物信息中心(NCBI)网站GeneBank上登录,登录号为:DQ385854,DQ388602～DQ388609。

钌(Ⅱ)多吡啶配合物与DNA相互作用研究

DNA是遗传信息的携带者和基因表达的物质基础,金属配合物与DNA的相互作用研究已受到广泛关注,成为生物无机化学的重要研究内容之一。本文简要评述了钌(Ⅱ)多吡啶配合物在DNA识别、断裂及拓扑异构酶抑制方面的研究情况。

手性双核钌(Ⅱ)配合物与DNA的相互作用研究

本文合成了1对手性双核钌(Ⅱ)配合物ΔΔ-和ΛΛ-[(bpy)2Ru(mbpibH2)Ru(bpy)2](ClO4)4(bpy=2,2′-联吡啶,mbpibH2=1,3-二(咪唑并[4,5-f][1,10-邻菲咯啉])苯)。通过元素分析、质谱、核磁共振、CD光谱对这两个化合物进行了结构表征。采用循环伏安法对配合物的电化学性质进行了分析。利用紫外-可见吸收光谱滴定、荧光光谱滴定、稳态荧光淬灭和粘度实验研究了配合物与DNA的相互作用,实验结果表明这2个配合物都能以插入的方式与DNA键合,而且ΔΔ配合物的DNA结合强度稍强于ΛΛ配合物。

一种含吲哚咪唑基Ru(Ⅱ)配合物的酸碱性质和与DNA相互作用的研究

合成了一个新的Ru(II)配合物[Ru(bpy)2(H2iip)](ClO4)2?5H2O[bpy=2,2'-联吡啶,H2iip=2-吲哚基-咪唑并[4,5-?][1,10]-邻菲罗啉].通过酸碱滴定发射光谱测定了该配合物的表观电离常数;用紫外可见光谱、荧光光谱、稳态荧光淬灭、溴化乙锭竞争键合、粘度测量和DNA裂解实验研究了配合物与DNA的相互作用性质.结果表明配合物以经典的插入模式与DNA键合,键合常数Kb=(5.97±0.27)×105mol-1?L(50mmol/LNaCl).