英语翻译在下感激不尽!1天内生效.AbstractApoptosis of cardiomyocytes followi

英语翻译
在下感激不尽!1天内生效.
Abstract
Apoptosis of cardiomyocytes following ischemia and
reperfusion is of clinical importance.However,little is
known about the mechanism by which it is induced.
-
Recently,essential roles of a Cl
channel whose activity
triggers the apoptotic volume decrease and of reactive
oxygen species (ROS) in activation of this channel have
been identified in mitochondrion-mediated apoptosis.
-
channels and
Therefore,in this study,involvement of Cl
ROS in apoptosis was studied in primary mouse
cardiomyocyte cultures subjected to ischemia-reperfusion.
Apoptotic cell death as measured by caspase-3 activation,
chromatin condensation,DNA laddering,and cell viability
reduction was observed tens of hours after reperfusion but
-
never immediately after ischemia.A non-selective Cl
channel blocker (DIDS or NPPB) rescued cells from
apoptotic death when applied during the reperfusion,but
not ischemia,period.Another blocker relatively specific to
-
the volume-sensitive outwardly rectifying (VSOR) Cl
channel (phloretin) was also effective in protecting ischemic
cardiomyocytes from apoptosis induced by reperfusion.A
profound increase in intracellular ROS was detected in
cardiomyocytes during the reperfusion,but not ischemia,
period.Scavengers for ROS,H O and superoxide all
2 2
inhibited apoptosis induced by ischemia-reperfusion.Thus,
it is concluded that the mechanism by which
cardiomyocyte apoptosis is induced by ischemia-
-
reperfusion involves VSOR Cl channel activity and
intracellular ROS production.

Abstract
文摘
Apoptosis of cardiomyocytes following ischemia and
心肌细胞的凋亡缺血后
reperfusion is of clinical importance.
再灌注的临床意义.
However, little is
然而,人们很少
known about the mechanism by which it is induced.
知道的机制是诱导.
-
——
Recently, essential roles of a Cl
最近,关键角色的一个Cl
channel whose activity
通道的活动
triggers the apoptotic volume decrease and of reactive
触发凋亡数量减少和活性
oxygen species (ROS) in activation of this channel have
氧物种(ROS)在激活这个频道都有
been identified in mitochondrion-mediated apoptosis.
被确认在mitochondrion-mediated凋亡.
-
——
channels and
渠道和
Therefore, in this study, involvement of Cl
因此,在这项研究中,参与的Cl
ROS in apoptosis was studied in primary mouse
ROS在凋亡研究主要鼠标
cardiomyocyte cultures subjected to ischemia-reperfusion.
心肌细胞的文化受到缺血再灌注.
Apoptotic cell death as measured by caspase-3 activation,
凋亡细胞死亡作为衡量caspase-3激活,
chromatin condensation, DNA laddering, and cell viability
染色质缩合、DNA阶梯,细胞活力
reduction was observed tens of hours after reperfusion but
观察减少数万小时后再灌注但
-
——
never immediately after ischemia.
从不立即缺血后.
A non-selective Cl
作为信条Cl
channel blocker (DIDS or NPPB) rescued cells from
通道阻滞剂(网络入侵检测系统或NPPB)获救的细胞
apoptotic death when applied during the reperfusion, but
当应用中凋亡死亡再灌注,但是
not ischemia, period.
没有缺血,时期.
Another blocker relatively specific to
另一个拦截器相对具体到
-
——
the volume-sensitive outwardly rectifying (VSOR) Cl
表面上的volume-sensitive整流(VSOR)Cl
channel (phloretin) was also effective in protecting ischemic
通道(得到)也是有效的保护缺血
cardiomyocytes from apoptosis induced by reperfusion.
从再灌注心肌细胞诱导细胞凋亡.
A
一个
profound increase in intracellular ROS was detected in
深刻的增加细胞内活性氧中被发现
cardiomyocytes during the reperfusion, but not ischemia,
在再灌注心肌细胞,但不是缺血,
period.
期.
Scavengers for ROS, H O and superoxide all
食腐动物对活性氧,H O和超氧化物所有
2 2
2
inhibited apoptosis induced by ischemia-reperfusion.
抑制缺血再灌注诱导细胞凋亡.
Thus,
因此,
it is concluded that the mechanism by which
得出的机制
cardiomyocyte apoptosis is induced by ischemia-
心肌细胞凋亡是诱导缺血-
-
——
reperfusion involves VSOR Cl channel activity and
再灌注涉及VSOR Cl通道活动和
intracellular ROS production.
细胞内活性氧产量.
文摘
心肌细胞的凋亡缺血后
再灌注的临床意义.
然而,人们很少
知道的机制是诱导.
——
最近,关键角色的一个Cl
通道的活动
触发凋亡数量减少和活性
氧物种(ROS)在激活这个频道都有
被确认在mitochondrion-mediated凋亡.
——
渠道和
因此,在这项研究中,参与的Cl
ROS在凋亡研究主要鼠标
心肌细胞的文化受到缺血再灌注.
凋亡细胞死亡作为衡量caspase-3激活,
染色质缩合、DNA阶梯,细胞活力
观察减少数万小时后再灌注但
——
从不立即缺血后.
作为信条Cl
通道阻滞剂(网络入侵检测系统或NPPB)获救的细胞
当应用中凋亡死亡再灌注,但是
没有缺血,时期.
另一个拦截器相对具体到
——
表面上的volume-sensitive整流(VSOR)Cl
通道(得到)也是有效的保护缺血
从再灌注心肌细胞诱导细胞凋亡.
一个
深刻的增加细胞内活性氧中被发现
在再灌注心肌细胞,但不是缺血,
期.
食腐动物对活性氧,H O和超氧化物所有
2
抑制缺血再灌注诱导细胞凋亡.
因此,
得出的机制
心肌细胞凋亡是诱导缺血-
——
再灌注涉及VSOR Cl通道活动和
细胞内活性氧产量.