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本文报道了阿克拉霉素B(ACM-B)对单纯疱疹病毒Ⅱ型(HSV-2)复制及其DNA聚合酶活性的影响。实验采用单层Vero细胞,空斑降低测定用来评价实验结果。加入ACM-B,明显地降低病毒空斑的形成。当ACM-B剂量大于0.3μm时,空斑数降低到零,表明ACM-B抑制HSV-2的复制。另外,ACM-B也抑制HSV-2诱导的DNA聚合酶活性。这提示,药物对HSV-2复制的抑制作用可能是由于对病毒DNA合成的抑制。吸收光谱分析证实,ACM-B能与活化DNA模板相互作用。ACM-B也抑制E.Coli DNA pol.Ⅰ及L1210DNA pol.α,证明ACM-B对HSV-2 DNApol.的抑制是非选择性的.ACM-B对HSV-2复制的抑制效应较ACM-A强,而细胞毒性效应也较后者为高。
This article reports the effect of aclacinomycin B (ACM-B) on herpes simplex virus type 2 (HSV-2) replication and its DNA polymerase activity. The experiment used monolayers of Vero cells and the plaque reduction assay was used to evaluate the experimental results. Addition of ACM-B significantly reduced the formation of viral plaques. When the dose of ACM-B is greater than 0.3 μm, the number of plaques is reduced to zero, indicating that ACM-B inhibits HSV-2 replication. In addition, ACM-B also inhibits HSV-2-induced DNA polymerase activity. This suggests that the inhibitory effect of the drug on HSV-2 replication may be due to the inhibition of viral DNA synthesis. Absorption spectroscopy confirmed that ACM-B interacts with the activated DNA template. ACM-B also inhibited E. coli DNA pol.Ⅰ and L1210 DNA pol.α, demonstrating that ACM-B inhibits the inhibition of HSV-2 DNApol. The inhibitory effect of ACM-B on HSV-2 replication is stronger than that of ACM-A Strong, while the cytotoxic effect is higher than the latter.