CAJ | 학술논문

目的观察青年和老年大鼠脑缺血后海马CA1区脑红蛋白(Ngb)表达的变化及肢体缺血预处理(LIP)对其影响. 方法将凝闭双侧椎动脉的青年和老年大鼠均随机分为脑缺血组和脑缺血+LIP组.采用反转录聚合酶链反应(RT-PCR)和Western blot法检测海马CA1区NgbmRNA和蛋白表达,硫堇染色观察海马CA1区锥体神经元迟发性死亡(DND)情况. 结果青年脑缺血组、青年脑缺血+LIP组、老年脑缺血组、老年脑缺血+LIP组的Ngb mRNA和蛋白表达分别为0.16±0.02和0.32±0.07、0.52±0.04和0.91±0.06、0.09±0.01和0.22±0.08、0.21±0.01和0.66±0.06.表明老年大鼠脑缺血后海马CA1区Ngb mRNA和蛋白表达较青年脑缺血大鼠降低(P<0.05),LIP可上调青年和老年大鼠脑缺血后海马CA1区Ngb mRNA和蛋白表达(P<0.05),但对老年大鼠的上调作用低于青年大鼠(P<0.05).硫堇染色显示,海马CA1区神经元密度青年脑缺血组,青年脑缺血+LIP组、老年脑缺血组和老年脑缺血+LIP组分别为(38.8±10.9)、(171.5±16.9)、(21.2±12.2)个/mm和(102.7±15.4)个/mm.表明老年大鼠LIP预防脑缺血引起的海马CA1区锥体神经元DND的作用小于青年大鼠. 结论老年大鼠脑缺血后Ngb的表达及LIP对其上调作用较青年大鼠明显减弱,这可能是老年大鼠脑缺血后损伤较重和LIP对老年大鼠脑缺血保护作用较弱的原因之一.
목적 관찰청년화노년대서뇌결혈후해마CA1구뇌홍단백(Ngb)표체적변화급지체결혈예처리(LIP)대기영향. 방법 장응폐쌍측추동맥적청년화노년대서균수궤분위뇌결혈조화뇌결혈+LIP조.채용반전록취합매련반응(RT-PCR)화Western blot법검측해마CA1구NgbmRNA화단백표체,류근염색관찰해마CA1구추체신경원지발성사망(DND)정황. 결과 청년뇌결혈조、청년뇌결혈+LIP조、노년뇌결혈조、노년뇌결혈+LIP조적Ngb mRNA화단백표체분별위0.16±0.02화0.32±0.07、0.52±0.04화0.91±0.06、0.09±0.01화0.22±0.08、0.21±0.01화0.66±0.06.표명노년대서뇌결혈후해마CA1구Ngb mRNA화단백표체교청년뇌결혈대서강저(P<0.05),LIP가상조청년화노년대서뇌결혈후해마CA1구Ngb mRNA화단백표체(P<0.05),단대노년대서적상조작용저우청년대서(P<0.05).류근염색현시,해마CA1구신경원밀도청년뇌결혈조,청년뇌결혈+LIP조、노년뇌결혈조화노년뇌결혈+LIP조분별위(38.8±10.9)、(171.5±16.9)、(21.2±12.2)개/mm화(102.7±15.4)개/mm.표명노년대서LIP예방뇌결혈인기적해마CA1구추체신경원DND적작용소우청년대서. 결론 노년대서뇌결혈후Ngb적표체급LIP대기상조작용교청년대서명현감약,저가능시노년대서뇌결혈후손상교중화LIP대노년대서뇌결혈보호작용교약적원인지일.
Objective To investigate the changes of neuroglobin (Ngb) expression in the CA1 hippocampus after cerebral ischemia and the effect of limb ischemic preconditioning (LIP) on it in young and aged rats. Methods SD rats aged 3 months and 21-23 months with permanently occluding bilateral vertebral arteries were randomly divided into cerebral ischemic group and LIP + cerebral ischemic group, respectively. The expression of Ngb mRNA and protein in the hippocampus were investigated by reverse transcription-polymerase chain reaction (RT-PCR) and Western blot methods. The profile of delayed neuronal death (DND) of pyramidal neurons in the hippocampus CA1 was evaluated by using thionin staining under light microscope by determining the neuronal density (ND) and histological grade (HG). Results Ngb mRNA and protein expressions were 0.16±0.02 and 0.32±0.07, 0.52±0.04 and 0.91±0.06, 0.09±0.01 and 0.22±0.08, 0.21±0.01 and 0.66± 0. 06 in young cerebral ischemia group, LIP + young cerebral ischemia group, aged cerebral ischemia group and LIP + aged cerebral ischemia group, respectively. The expressions of Ngb mRNA and protein after cerebral ischemia for 8 minutes in aged rats were decreased compared with those in the young rats which suffered an identical cerebral ischemia with the aged rats (P<0.05). LIP up-regulated Ngb mRNA and protein expressions in both young and aged rats which suffered cerebral ischemia (P<0.05). However, the up-regulation of Ngb expression in aged rats was significantly less than that in young rats (P<0.05). Neuropathological evaluation showed that ND was 38.8±10.9, 171.5±16.9, 21.2±12.2 and 102.7±15.4 in young cerebral ischemic group, LIP + young cerebral ischemic group, aged cerebral ischemic group and LIP + aged cerebral ischemic group, respectively. It showed that obvious DND of pyramidal neurons was found in young and aged rats after cerebral ischemia. Although LIP effectively protected the pyramidal neurons in the CA1 hippocampus against DND normally induced by ischemic insult, the neuroprotection of LIP for aged rats was less effective than that for young rats. Conclusions The expression of Ngb and the up-regulation effect of LIP on the expression in aged rats are significantly decreased compared to those in young rats when the rats suffer cerebral ischemia. These differences may be one of underlying reasons why the aged rats exhibit severe DND after cerebral ischemia and why the neuroprotective effect of LIP is less in the aged rats than that in the young rats.