Saito T, Tanaka M, Yamaguchi I
Department of Animal Science, Faculty of Agriculture, Kobe University, Japan.
J Vet Med Sci. 1996 Nov;58(11):1137-9. doi: 10.1292/jvms.58.11_1137.
Effect of brefeldin A (BFA) on influenza virus-infected cells was examined by measuring cell viability, microscopic examination, and DNA fragmentation analysis. When Madin-Darby canine kidney (MDCK) cells were infected with influenza A virus together with BFA treatment, virus-induced cell death was observed earlier than in the virus-infected cells without BFA treatment. By microscopic examination, the mode of cell death in virus-infected cells with BFA treatment appeared different from that of the cells without BFA treatment. Because influenza virus causes apoptosis in the host cells, extent of DNA fragmentation was compared between virus-infected cells with and without BFA treatment. BFA treatment resulted in inhibition of DNA fragmentation of virus-infected cells. Treatment of virus-infected cells with anti-oxidant (10 mM N-acetyl-L-cysteine) also inhibited DNA fragmentation of influenza virus-infected cells. A possible mechanism of BFA affecting influenza virus-induced apoptosis is discussed.
通过测量细胞活力、显微镜检查和DNA片段化分析，研究了布雷菲德菌素A（BFA）对流感病毒感染细胞的影响。当用BFA处理的同时用甲型流感病毒感染麦迪逊-达比犬肾（MDCK）细胞时，观察到病毒诱导的细胞死亡比未用BFA处理的病毒感染细胞更早出现。通过显微镜检查，用BFA处理的病毒感染细胞的细胞死亡模式似乎与未用BFA处理的细胞不同。由于流感病毒会导致宿主细胞凋亡，因此比较了用BFA处理和未用BFA处理的病毒感染细胞之间的DNA片段化程度。BFA处理导致病毒感染细胞的DNA片段化受到抑制。用抗氧化剂（10 mM N-乙酰-L-半胱氨酸）处理病毒感染细胞也抑制了流感病毒感染细胞的DNA片段化。讨论了BFA影响流感病毒诱导凋亡的可能机制。
