...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Alcohol >Role of protein kinase C in estrogen protection against apoptotic cerebellar cell death in ethanol-withdrawn rats.
【24h】

Role of protein kinase C in estrogen protection against apoptotic cerebellar cell death in ethanol-withdrawn rats.

机译：蛋白激酶C在雌性激素抵抗乙醇撤除大鼠的凋亡小脑细胞死亡中的作用。

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

Results of studies from our laboratory have shown that administration of 17beta-estradiol (E(2)) reduces cerebellar neuronal damage during ethanol withdrawal (EW). In the current study, we examined mechanisms underlying E(2) protection against EW-associated cerebellar damage by assessing apoptotic indicators: DNA fragmentation, caspase-3 activity, and protein kinase C (PKC) activity. Ovariectomized rats, implanted with E(2) or oil pellets, received ethanol [7.5% weight/volume (wt./vol.)] (EW/E(2) group and EW/Oil group, respectively) chronically (for 5 weeks) or control dextrin diet (Dextrin/Oil group). At day 14 of EW, cerebelli were collected for the terminal deoxynucleotidyltransferase (TdT)-mediated dUDP-biotin nick end labeling (TUNEL) assay to detect DNA fragmentation and for immunohistochemistry to detect caspase-3 activation. A separate group of rat cerebelli was prepared to assess for total PKC activity, as well as for activity of a specific PKC isozyme, epsilon (PKCepsilon), by using an in vitro [gamma-(32)P]ATP phosphorylation assay at days 1 and 14 of EW. Results indicated that rats in the EW/Oil group had more DNA fragments and caspase-3-positive neuronal cells than observed for control rats, and these effects were inhibited by E(2) treatment. For total PKC activity at day 1 of EW, rats in the EW/E(2) group had a lower cytosolic PKC activity than observed for either rats in the EW/Oil group or control rats. At day 14 of EW, both EW groups had a lower total PKC activity than observed for control rats. For PKCepsilon activity, rats in the EW/E(2) group had a lower cytosolic PKCepsilon activity than observed for rats in the EW/Oil group or for control rats at day 1, and they had a lower membrane PKCepsilon activity at day 14 of EW than observed for control rats. These findings support the suggestion that E(2) protects against cerebellar neuronal damage in ethanol-withdrawn rats by inhibition of DNA fragmentation and caspase-3 activation, and that reduced PKC activity may be involved in the protection.
机译：我们实验室的研究结果表明，服用17β-雌二醇（E（2））可以减少乙醇戒断（EW）期间小脑神经元的损害。在当前的研究中，我们通过评估凋亡指标：DNA片段化，caspase-3活性和蛋白激酶C（PKC）活性，检查了针对E（2）对抗EW相关小脑损伤的潜在保护机制。卵巢切除的大鼠植入了E（2）或油丸，接受了乙醇（分别为EW / E（2）组和EW / Oil组）[7.5％重量/体积（重量/体积）]乙醇（持续5周） ）或控制糊精饮食（糊精/油脂组）。在EW的第14天，收集小脑用于末端脱氧核苷酸转移酶（TdT）介导的dUDP-生物素缺口末端标记（TUNEL）分析，以检测DNA片段化，并进行免疫组织化学，以检测caspase-3活化。通过在第1天使用体外[γ-（32）P] ATP磷酸化测定，准备了另一组大鼠小脑以评估总PKC活性以及特定PKC同工酶epsilon（PKCepsilon）的活性。和EW的14。结果表明，EW / Oil组的大鼠比对照组的大鼠具有更多的DNA片段和caspase-3阳性神经元细胞，并且这些作用被E（2）处理抑制。对于EW第1天的总PKC活性，EW / E（2）组的大鼠的胞浆PKC活性低于EW / Oil组或对照组的大鼠。在EW的第14天，两个EW组的总PKC活性均低于对照大鼠。对于PKCepsilon活性，EW / E（2）组的大鼠的胞浆PKCepsilon活性低于EW / Oil组的大鼠或对照组的第1天，而它们的膜PKCepsilon活性在第14天较低。 EW比对照组大鼠观察到的要高。这些发现支持这样的建议，即E（2）通过抑制DNA片段化和caspase-3活化来保护乙醇撤回大鼠免受小脑神经元损害，并且降低的PKC活性可能参与了这种保护。

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