中华老年医学杂志
中華老年醫學雜誌
중화노년의학잡지
Chinese Journal of Geriatrics
2009年
1期
74-77
,共4页
脑缺血%原肌球蛋白%受体蛋白质酪氨酸激酶类%蛋白激酶类%神经生长因子
腦缺血%原肌毬蛋白%受體蛋白質酪氨痠激酶類%蛋白激酶類%神經生長因子
뇌결혈%원기구단백%수체단백질락안산격매류%단백격매류%신경생장인자
Cerebral lschemia%Tropomyosin%Receptor protein-tyrosine kinases%Protein kinases%Nerve growth factor
目的 观察脑缺血后原肌球蛋白受体激酶(Trk)和蛋白激酶B(Akt)信号蛋白的动态变化规律,同时观察β-神经生长因子(β-NGF)对其影响,探讨β-NGF脑缺血保护的作用机制. 方法制作大鼠局灶性脑缺血模型,腹腔注射β-NGF,应用免疫组化和Western印迹法检测Trk及Akt磷酸化的变化. 结果缺血8 h后Trk受体在半暗带表达增加.缺血2 h后Trk磷酸化即丌始不断增加,Akt的磷酸化则先减少,后逐渐恢复,其中缺血8 h较正常对照组减少了76.5%(P<0.01).注射β-NGF后在缺血12 h,Trk磷酸化水平增加了 74.4%(P<0.01);Akt磷酸化水平在缺血8 h时明显恢复,在24 h 与正常对照组比较差异无统计学意义(P>0.05). 结论脑缺血促使Trk受体表达增加与激活.β-NGF可能通过增强Trk磷酸化及调节Akt磷酸化发挥脑缺血保护作用.
目的 觀察腦缺血後原肌毬蛋白受體激酶(Trk)和蛋白激酶B(Akt)信號蛋白的動態變化規律,同時觀察β-神經生長因子(β-NGF)對其影響,探討β-NGF腦缺血保護的作用機製. 方法製作大鼠跼竈性腦缺血模型,腹腔註射β-NGF,應用免疫組化和Western印跡法檢測Trk及Akt燐痠化的變化. 結果缺血8 h後Trk受體在半暗帶錶達增加.缺血2 h後Trk燐痠化即丌始不斷增加,Akt的燐痠化則先減少,後逐漸恢複,其中缺血8 h較正常對照組減少瞭76.5%(P<0.01).註射β-NGF後在缺血12 h,Trk燐痠化水平增加瞭 74.4%(P<0.01);Akt燐痠化水平在缺血8 h時明顯恢複,在24 h 與正常對照組比較差異無統計學意義(P>0.05). 結論腦缺血促使Trk受體錶達增加與激活.β-NGF可能通過增彊Trk燐痠化及調節Akt燐痠化髮揮腦缺血保護作用.
목적 관찰뇌결혈후원기구단백수체격매(Trk)화단백격매B(Akt)신호단백적동태변화규률,동시관찰β-신경생장인자(β-NGF)대기영향,탐토β-NGF뇌결혈보호적작용궤제. 방법제작대서국조성뇌결혈모형,복강주사β-NGF,응용면역조화화Western인적법검측Trk급Akt린산화적변화. 결과결혈8 h후Trk수체재반암대표체증가.결혈2 h후Trk린산화즉기시불단증가,Akt적린산화칙선감소,후축점회복,기중결혈8 h교정상대조조감소료76.5%(P<0.01).주사β-NGF후재결혈12 h,Trk린산화수평증가료 74.4%(P<0.01);Akt린산화수평재결혈8 h시명현회복,재24 h 여정상대조조비교차이무통계학의의(P>0.05). 결론뇌결혈촉사Trk수체표체증가여격활.β-NGF가능통과증강Trk린산화급조절Akt린산화발휘뇌결혈보호작용.
Objective To investigate the dynamic changes of Trk(tropomyosin receptor kinase) and Akt(protein kinase B), and to explore the neuroprotective role and its mechanism of β-NGF (β-nerve growth factor) after focal cerebral ischemia. Methods A focal cerebral ischemia rat model was made and β-NGF was injected intra abdominally. The phosphorylation of Trk and Akt were tested by immunocytochemistry and Western blot assay. Results Trk receptor was increased obviously in the penumbra area after 8 h of infarction. The level of phosphorylated Trk(p-Trk) was increased after 2 h of infarction, while the level of phosphorylated Akt(p-Akt) had a decrease and then recovered gradually. The level of p Akt in cerebral ischemia group was decreased by 76.5% compared with that in control group after 8 h of infarction(P<0. 01). After the injection of β-NGF, the level of p-Trk was increased by 74.4% after 12 h of infarction(P<0.01), while the level of p-Akt was recovered significantly after 8 h of infarction, and had no statistical difference compared with the control group after 24 h of infarction (P>0.05). Conclusions Ischemia induces the activation and increased expression of Trk receptor, andβ-NGF may play a protective role in cerebral ischemia by increasing the phosphorylation of Trk and regulating the phosphorylation of Akt.
