The anti-herpetic activity of trichosanthin via the nuclear factor-¦ÊB and p53 pathways

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• 作者：Dongxu He^a ; Yongtang Zheng^b ; Siucheung Tam^c ; ^{MTAM@cuhk.edu.hk}
• 关键词：Trichosanthin ; Human herpes simplex virus type 1 ; Nuclear factor-¦ÊB ; p53
• 刊名：Life Sciences
• 出版年：2012
• 出版时间：15 May, 2012
• 年：2012
• 卷：90
• 期：17-18
• 页码：673-681
• 全文大小：1345 K

文摘

Aims

Trichosanthin (TCS) is a type I ribosome-inactivating protein. We have previously shown that TCS induces a more potent apoptosis in infected cells over uninfected cells, but the mechanism underlying it is unclear. In this study, we explored the anti-HSV-1 mechanism of TCS through the nuclear factor-¦ÊB (NF-¦ÊB) and p53 pathways in human epithelial carcinoma (HEp-2) cells with wild type p53.

Main methods

The western blot, electrophoretic mobility shift assay, chromatin immunoprecipitation assay, enzyme-linked immunosorbent assay and cytokinesis-block micronucleus were applied in this study.

Key findings

It was shown that TCS inhibited the HSV-1-induced NF-¦ÊB activation. Meanwhile, in HSV-1 infected cells, TCS treatment activated significantly more p53 and BAX, with no DNA damage and less S phase arrest compared with uninfected cells. The activation of BAX in infected cells correlated with the cell death signaling of p53.

Significance

Taken together, these results suggest that the anti-HSV-1 effect of TCS is related to its suppression of NF-¦ÊB activation and regulation of p53-dependent cell death in infected cells.