基础医学与临床
基礎醫學與臨床
기출의학여림상
BASIC MEDICAL SCIENCES AND CLINICS
2010年
1期
1-5
,共5页
李海涛%江君%杨巍巍%卜祥宁%韩松%李俊发
李海濤%江君%楊巍巍%蔔祥寧%韓鬆%李俊髮
리해도%강군%양외외%복상저%한송%리준발
低氧预适应%CaMKⅡ%海马%皮层
低氧預適應%CaMKⅡ%海馬%皮層
저양예괄응%CaMKⅡ%해마%피층
HPC%CaMKⅡ%hippocampus%cortex
目的 探讨钙调蛋白依赖性蛋白激酶(CaMKⅡ)在小鼠脑低氧预适应(HPC)发生发展中的作用.方法 成年雄性BALB/c小鼠随机分为正常对照(H0)、早期(H1~H4)和延迟性(H5~H6)低氧预适应等共计7组,制备小鼠HPC模型;用Western blot并结合Gel Doc凝胶成像系统,检测小鼠脑组织内CaMKⅡ磷酸化水平和蛋白表达量;用免疫组化检测小鼠脑皮层和海马CaMKⅡ磷酸化水平.结果 与H0组小鼠相比,H3~H5组海马和皮层的CaMKⅡ磷酸化水平明显升高(P<0.05);而H1~H6组的皮层和海马的CaMKⅡ蛋白表达量无明显变化;H3、H6组皮层和海马p-CaMKⅡ阳性细胞数目增多和灰度增强.结论 CaMKⅡ磷酸化水平的升高可能参与了小鼠脑HPC的发生发展过程.
目的 探討鈣調蛋白依賴性蛋白激酶(CaMKⅡ)在小鼠腦低氧預適應(HPC)髮生髮展中的作用.方法 成年雄性BALB/c小鼠隨機分為正常對照(H0)、早期(H1~H4)和延遲性(H5~H6)低氧預適應等共計7組,製備小鼠HPC模型;用Western blot併結閤Gel Doc凝膠成像繫統,檢測小鼠腦組織內CaMKⅡ燐痠化水平和蛋白錶達量;用免疫組化檢測小鼠腦皮層和海馬CaMKⅡ燐痠化水平.結果 與H0組小鼠相比,H3~H5組海馬和皮層的CaMKⅡ燐痠化水平明顯升高(P<0.05);而H1~H6組的皮層和海馬的CaMKⅡ蛋白錶達量無明顯變化;H3、H6組皮層和海馬p-CaMKⅡ暘性細胞數目增多和灰度增彊.結論 CaMKⅡ燐痠化水平的升高可能參與瞭小鼠腦HPC的髮生髮展過程.
목적 탐토개조단백의뢰성단백격매(CaMKⅡ)재소서뇌저양예괄응(HPC)발생발전중적작용.방법 성년웅성BALB/c소서수궤분위정상대조(H0)、조기(H1~H4)화연지성(H5~H6)저양예괄응등공계7조,제비소서HPC모형;용Western blot병결합Gel Doc응효성상계통,검측소서뇌조직내CaMKⅡ린산화수평화단백표체량;용면역조화검측소서뇌피층화해마CaMKⅡ린산화수평.결과 여H0조소서상비,H3~H5조해마화피층적CaMKⅡ린산화수평명현승고(P<0.05);이H1~H6조적피층화해마적CaMKⅡ단백표체량무명현변화;H3、H6조피층화해마p-CaMKⅡ양성세포수목증다화회도증강.결론 CaMKⅡ린산화수평적승고가능삼여료소서뇌HPC적발생발전과정.
Objective To explore the role of calcium/calmodulin-dependent protein kinase Ⅱ ( CaMK Ⅱ ) in the development of cerebral hypoxic preconditioning(HPC). Methods Healthy male BALB/c mice were randomly divided into 7 groups as follows; normoxic control (H0) , early(H1~H4) and delayed (H5~H6) hypoxically preconditioned mice groups. SDS-PAGE, Western blot and Gel Doc imagine systems were applied to quantitatively analyze the level of CaMK Ⅱ phosphorylation and protein expression level in the brain of mice. Results Compared with H0 group, the phosphorylation level of CaMK Ⅱ increased in cortex and hippocampus of mice in H3~H5 hypoxically preconditioned groups (P<0.05). However, there was no significant changes in total CaMK Ⅱ protein expression in cortex and hippocampus of hypoxic preconditioned mice. Similarly, enhanced p-Thr286 CaMK Ⅱ was also observed in the hippocampus and cortex of mice by immunostaining following hypoxic exposures (H3 and H6). Conclusion The increased phosphorylation of CaMKⅡ may be involved in the development of cerebral HPC in mice.