摘要
目的:探讨大鼠视网膜缺血再灌注损伤后bcl-2和baxmRNA的表达变化及其意义。方法:采用升高眼内压的方法,制作实验性视网膜缺血再灌注大鼠模型。将30只Wistar大鼠随机分为正常组(n=4)和缺血再灌注组(n=16),其中缺血再灌注组又分为再灌注后2、6、24、72h等4个时间段(每时间段4只)。应用反转录聚合酶链式反应(RT-PCR)法检测视网膜组织中bcl-2和baxmRNA的表达变化。结果:视网膜组织内bcl-2mRNA的表达水平在缺血再灌注损伤后2h时即开始下降,6h时降至最低,持续至第72h,与正常组相比有显著差异(P<0.01)。与bcl-2的表达相反,baxmRNA的表达呈上升趋势,6h时达最高,72h时仍显著高于正常组(P<0.01)。结论:bcl-2和bax可能参与了缺血再灌注损伤所造成的视网膜细胞的凋亡过程。
Objective To investigate the changes in expression of bcl-2 and bax mRNA after ischemia-reperfusion injury in rat retina and its significance.Method The rat model of experimental ischemia-reperfusion injury in retina was made by method of increasing intraocular pressure.30 Wistar rats were divided into the normal group（n=4） and the ischemia-reperfusion injury group（n=16）.The latter group was subdivided into four time points as 2,6,24 and 72 h after reperfusion（n=4/time point）.The expression of bcl-2 and bax mRNA in rat retina was detected by reverse transcriptase-polymerase chain reaction（RT-PCR） technique. Results The expression level of bcl-2 mRNA in rat retina began to decrease 2h after ischemia-reperfusion injury, reached to the lowest at 6h,and lasted to 72h,and was significantly different with that in the normal group（P〈0.01）.In contrast to the expression of bcl-2,the expression of bax mRNA increased after ischemia-reperfusion,reached the peak at 6h,and kept a higher level to 72h,also had significant difference with the normal group（P〈0.01）. Conclusion Bcl-2 and bax may involve in the apoptotic process of retina neurons induced by ischemia-reperfusion injury.
出处
《吉林医学》
CAS
2007年第13期1452-1454,共3页
Jilin Medical Journal
