Kagohashi Yukiko, Naora Hiroyuki, Otani Hiroki
Department of Anatomy, Shimane Medical University, Izumo 693-8501, Japan.
Congenit Anom (Kyoto). 2002 Mar;42(1):15-20. doi: 10.1111/j.1741-4520.2002.tb00849.x.
We previously showed that PSK, a biological response modifier, suppressed X-ray irradiation induced ocular anomalies in mouse embryos. In the present study, in mouse embryos irradiated at E7.5, PSK, when administered immediately after irradiation, suppressed mitosis and increased apoptosis as compared with embryos not treated with PSK at 12 hrs after irradiation. In the irradiated embryos, p53, which is normally expressed at a high level in early embryos, increased at 6 hrs and decreased at 12 hrs after irradiation. In the irradiated and PSK-treated embryos, the p53 level did not change at 6 hrs, increased at 12 hrs and decreased at 24 hrs after irradiation. This timing of PSK-induced delayed increase of p53 coincided with that of the PSK-induced decrease in mitosis and increase in apoptosis. These results suggested that PSK modified the p53 level and affected cell proliferation and apoptosis, which might contribute to the suppression of teratogenesis.
我们之前表明,生物反应调节剂PSK可抑制X射线照射诱导的小鼠胚胎眼部异常。在本研究中,对于在E7.5时接受照射的小鼠胚胎,与照射后12小时未用PSK处理的胚胎相比,照射后立即给予PSK可抑制有丝分裂并增加细胞凋亡。在受照射的胚胎中,正常情况下在早期胚胎中高水平表达的p53在照射后6小时增加,在照射后12小时减少。在受照射并经PSK处理的胚胎中,p53水平在照射后6小时没有变化,在照射后12小时增加,在照射后24小时减少。PSK诱导的p53延迟增加的时间与PSK诱导的有丝分裂减少和细胞凋亡增加的时间一致。这些结果表明,PSK改变了p53水平并影响细胞增殖和凋亡,这可能有助于抑制致畸作用。