...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Journal of biochemical and molecular toxicology >Tumor necrosis factor alpha-mediated activation of c-Jun NH(2)-terminal kinase as a mechanism for fumonisin B(1) induced apoptosis in murine primary hepatocytes.
【24h】

Tumor necrosis factor alpha-mediated activation of c-Jun NH(2)-terminal kinase as a mechanism for fumonisin B(1) induced apoptosis in murine primary hepatocytes.

机译：肿瘤坏死因子α介导的c-Jun NH（2）端激酶激活作为伏马毒素B（1）的机制诱导鼠原代肝细胞凋亡。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Fumonisin B(1) is a mycotoxin produced by Fusarium verticillioides, frequently associated with corn. It produces species-specific and organ-specific toxicity, including equine leukoencephalomalacia, porcine pulmonary edema, and hepatic or renal damage in most animal species. Fumonisin B(1) perturbs sphingolipid metabolism by inhibiting ceramide synthase. Our previous studies indicated that fumonisin B(1) caused localized activation of cytokines in liver produced by macrophages and other cell types that modulate fumonisin B(1) induced hepatic apoptosis in mice. The role of tumor necrosis factor alpha (TNFalpha) in fumonisin B(1) mediated hepatocyte apoptosis has been established; not much is known about the downstream events leading to apoptosis. In the current study, fumonisin B(1) induced apoptosis in primary culture of liver cells. In consistence with previous reports, fumonisin B(1) caused accumulation of sphingoid bases and led to increase in TNFalpha expression. Phosphorylated and total c-Jun NH(2)-terminal kinase (JNK) activities were increased after 24 h fumonisin B(1) treatment. JNK inhibitor (SP600125) and anti-TNFalpha reduced the apoptosis induced by fumonisin B(1). The role of JNK signaling in fumonisin B(1) induced apoptosis is downstream of TNFalpha production, as fumonisin B(1)-mediated activation of JNK was reduced by the presence of anti-TNFalpha in the medium, whereas the presence of JNK inhibitor did not change the fumonisin B(1) induced TNFalpha expression. Results of this study imply that generation of fumonisin B(1) induced TNFalpha results in modulation of mitogen activated protein kinases, particularly of JNK, and provides a possible mechanism for apoptosis in murine hepatocytes.
机译：伏马菌素B（1）是由镰刀菌（Fusarium v​​erticillioides）产生的霉菌毒素，通常与玉米有关。它产生物种特异性和器官特异性毒性，包括大多数动物物种的马脑白质软化症，猪肺水肿以及肝或肾损害。伏马菌素B（1）通过抑制神经酰胺合酶扰动鞘脂代谢。我们以前的研究表明，伏马毒素B（1）引起巨噬细胞和其他调节伏马毒素B（1）诱导小鼠肝细胞凋亡的细胞类型产生的肝细胞因子的局部激活。已经建立了肿瘤坏死因子α（TNFalpha）在伏马毒素B（1）介导的肝细胞凋亡中的作用;关于导致细胞凋亡的下游事件知之甚少。在当前的研究中，伏马毒素B（1）诱导肝细胞原代培养细胞凋亡。与以前的报告一致，伏马毒素B（1）引起了类鞘氨醇碱基的积累，并导致TNFalpha表达增加。伏马菌素B（1）处理24小时后，磷酸化和总c-Jun NH（2）端激酶（JNK）活性增加。 JNK抑制剂（SP600125）和抗TNFα降低了伏马菌素B（1）诱导的细胞凋亡。 JNK信号在伏马毒素B（1）诱导的凋亡中的作用是TNFalpha的下游，因为在培养基中抗TNFalpha的存在降低了伏马毒素B（1）介导的JNK激活，而JNK抑制剂的存在确实不会改变伏马毒素B（1）诱导的TNFalpha表达。这项研究的结果表明，伏马菌素B（1）诱导的TNFα的产生导致有丝分裂原激活的蛋白激酶，特别是JNK的调节，并为鼠肝细胞凋亡提供了可能的机制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号