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目的 研究小分子化合物大环多胺类MP A、MP B和MP C抗人类免疫缺陷病毒 (HIV) 1的生物活性机制。方法 通过核酸Tm测定及圆二色 (CD)光谱法观察大环多胺类化合物对聚腺尿苷酸PolyA∶PolyU构象的影响 ;核酸断裂实验用琼脂糖凝胶电泳法、流式细胞计数法研究其对细胞凋亡和周期的影响 ;计算机分子模型Docking计算从理论上判断其与TARRNA结合的可能性。 结果 ①MP A、MP B和MP C不仅可引起PolyA∶PolyU构象的变化使其发生断裂 ,而且可抑制Tat RNA相互结合。②MP A、MP B和MP C可影响细胞亚二倍体的含量。③分子模型理论计算结果与实验结果基本一致。结论 大环多胺MP A、MP B和MP C可能通过与病毒基因组RNA的作用抑制HIV 1RNA与Tat蛋白的结合而发挥抗HIV 1的活性。
Objective To study the biological activities of macrocyclic polyamines MP A, MP B and MP C against human immunodeficiency virus (HIV) 1. Methods The conformations of polyA: PolyU macromolecular polyamines were observed by Tm and CD spectroscopy. Nucleic acid cleavage experiments were performed by agarose gel electrophoresis and flow cytometry To study its effect on apoptosis and cycle; computer molecular model Docking calculation theoretically determine the possibility of its binding to TARRNA. Results ① MP A, MP B and MP C could not only cause the change of the conformation of PolyA: PolyU to break, but also inhibit the binding of Tat RNA. MP A, MP B and MP C can affect the cell sub-diploid content. ③ molecular model theory and experimental results are basically the same. Conclusion Macrocyclic polyamines MP A, MP B and MP C may exert anti-HIV 1 activity by inhibiting the binding of HIV 1 RNA and Tat protein with the action of viral genomic RNA.