Effect of vitamin E on hepatic cell proliferation and apoptosis in mice deficient in the p50 subunit of NF-κB after treatment with phenobarbital.

Effect of vitamin E on hepatic cell proliferation and apoptosis in mice deficient in the p50 subunit of NF-κB after treatment with phenobarbital.
复制标题

DOI:
10.1016/j.fct.2011.06.059
复制
发表时间:
2011-10
影响因子:
4.3
通讯作者:
Glauert, Howard P.
Glauert, Howard P.
中科院分区:
农林科学2区
文献类型:
--
作者:
Li, Jun;Harp, Casey;Tharappel, Job C.;Spear, Brett T.;Glauert, Howard P.

文献摘要

参考文献

相似文献

苯巴比妥(PB)是一种有效的肝肿瘤促进剂,研究较多。核因子κB(NF-κB)是一种由活性氧激活的转录因子,参与细胞增殖和凋亡。我们以前发现PB激活NF-κB,膳食维生素E可有效降低PB诱导的NF-κB DNA结合。因此,我们假设膳食维生素E通过其对NF-κB的作用影响PB诱导的细胞增殖和凋亡的变化。对NF-κB1缺陷小鼠(p50−/−)和野生型B6129小鼠喂食含有10或250 ppm维生素E(α-生育酚乙酸酯)的纯化饲料28天。在那个时候,一半的野生型和一半的p50−/−小鼠被置于相同的饮食与0.05%的PB 10天。与野生型小鼠相比,p50−/−小鼠的细胞增殖和凋亡水平更高。PB可显著促进细胞增殖,但维生素E对肝细胞增殖无影响。PB组细胞凋亡无明显变化,对照组和高维生素E组细胞凋亡无明显差异。因此,维生素E似乎不会影响野生型或p50−/−小鼠的细胞生长参数。
Phenobarbital (PB) is an efficacious and well-studied hepatic tumor promoting agent. Nuclear factorκB (NF-κB) is a transcription factor activated by reactive oxygen and is involved in cell proliferation and apoptosis. We previously found that PB activates NF-κB and that dietary vitamin E is effective in decreasing PB-induced NF-κB DNA binding. We therefore hypothesized that dietary vitamin E influences PB-induced changes in cell proliferation and apoptosis through its action on NF-κB. NF-κB1 deficient mice (p50−/−) and wild-type B6129 mice were fed a purified diet containing 10 or 250 ppm vitamin E (α-tocopherol acetate) for 28 days. At that time, half of the wild-type and half of the p50−/− mice were placed on the same diet with 0.05% PB for 10 days. Compared to wild-type mice, the p50−/− mice had higher levels of cell proliferation and apoptosis. Cell proliferation was significantly increased by PB, but vitamin E did not affect hepatic cell proliferation. Apoptosis was not changed in mice fed PB, and there was no significant difference in apoptosis between control and high vitamin E treated mice. Thus, vitamin E does not appear to influence cell growth parameters in either wild-type or p50−/− mice.
DOI: 10.1016/j.etap.2007.10.025
发表时间: 2008-03-01
影响因子: 4.3
作者:
Glauert, Howard P.;Tharappel, Job C.;Spear, Brett T.
通讯作者: Spear, Brett T.
DOI: 10.1093/carcin/8.10.1491
发表时间: 1987-10-01
期刊: CARCINOGENESIS
影响因子: 4.7
作者:
PITOT, HC;GOLDSWORTHY, TL;CAMPBELL, HA
通讯作者: CAMPBELL, HA
DOI: 10.1093/toxsci/kfg201
发表时间: 2003-10-01
影响因子: 3.8
作者:
Tharappel, JC;Nalca, A;Spear, BT
通讯作者: Spear, BT
DOI: 10.1006/bbrc.1996.1911
发表时间: 1996-12-24
影响因子: 3.1
作者:
Li, YX;Leung, LK;Glauert, HP
通讯作者: Glauert, HP
DOI: 10.1155/2008/286249
发表时间: 2008
期刊: PPAR RESEARCH
影响因子: 2.9
作者:
Glauert, Howard P.;Calfee-Mason, Karen;Li, Yixin;Nilakantan, Vani;Twaroski, Michelle L.;Tharappel, Job;Spear, Brett T.
通讯作者: Spear, Brett T.