
浏览全部资源
扫码关注微信
1. 重庆医科大学附属第一医院妇产科
2. 重庆医科大学附属第一医院妇产科,重庆,400016
纸质出版日期:2006,
扫 描 看 全 文
[1]张华,赵泽燕,张建华.2-脱氧葡萄糖对宫内窘迫所致胎鼠脑损伤的影响[J].重庆医科大学学报,2006(03):349-353.
HUANG Yan, et al. The influence of preconditioning on the activity of NF-κB and its myocardial protective effects[J]. Journal of Chongqing Medical University, 2006,(3):349-353.
目的:探讨宫内缺氧对海马神经元的影响及2-脱氧葡萄糖(2-deoxyglucose
2DG)的保护作用。方法:(1)建立胎鼠宫内窘迫模型。(2)实验动物分成正常组、假手术组、缺血再灌注组及治疗组。(3)检测胎鼠脑组织海马神经元的形态学改变及凋亡情况。结果:(1)正常组和假手术组异常细胞数量无显著差异(P>0.05)。缺血再灌注组与正常组及假手术组各相应时间点比较
异常细胞数量明显增多(P<0.05)。治疗组各时间点异常细胞数量与缺血再灌注组比较明显减少(P<0.05)。(2)正常组及假手术组胎鼠海马回CA1区锥体细胞密度无明显差异(P>0.05)。缺血再灌注组与正常组及假手术组比较
锥体细胞明显稀疏
随时间延长病变更加显著。治疗组与缺血再灌注组各相应时间点比较
存活锥体细胞密度均明显增加(P<0.05)。(3)缺血再灌注组再灌注3hTUNEL阳性细胞数目明显增多;至再灌注24h阳性神经元数量达最大值。治疗组海马回CA1区典型TUNEL阳性神经元数量与缺血再灌注组各相应时间点比较明显减少(P<0.05)。结论:宫内窘迫引起胎鼠海马神经元损伤
并与缺血再灌注的时间密切相关。而2DG对缺血缺氧引起的神经元损伤有明显的保护作用。
Objective: To investigate the influence of ischemic and pinacidil preconditioning on the activity of NF-κB and its myocardial protective effects.Methods: Eighty isolated rabbit hearts were randomized into five groups(Group C?K?I?P?G).Hearts were removed and mounted in a Langendorff apparatus perfused with 37℃ oxygenated Krebs-Henselet buffer.All groups were subjected to gobal myocardial ischemia for 40 min and reperfusion for 60 min or 120 min.Cardiac functions were monitored at 10 min equilibration ?15 min?30 min?60 min and 120 min reperfusion;Coronary flow(CF) was measured at 10 min equilibration and 30 min reperfusion;Expression of NF-κB P65 was determined at 10 min equilibration?60 min and 120min reperfusion.Results:(1)After ischemic reperfusion
the recovery of cardiac function and CF in Group I and Group P was significantly superior to that in Group C and Group K(P<0.01 or P<0.05);(2) The expression of NF-κB P65 in Group I and Group P was greater than that in Group C and Group P;The expression of NF-κB P65 in Group G were higher than that in Group P(P<0.05).Conclusion: Both ischemic and pinacidil preconditioning can protect myocardium from myocardial inflammation during ischemic reperfusion
the mechanisms of which may be that the opening sensitive potassium channel might have inhibited the activation of NF-κB directly or indirectly.
宫内窘迫胎鼠缺血缺氧性脑损伤2-脱氧葡萄糖
Ischemic/reperfusion injuryPreconditioningATP sensitive potassium channelNuclear factor-κappa B
0
浏览量
63
下载量
6
CSCD
关联资源
相关文章
相关作者
相关机构
京公网安备11010802024621