广州医学院学报
廣州醫學院學報
엄주의학원학보
ACADEMIC JOURNAL OF GUANGZHOU MEDICAL COLLEGE
2014年
2期
1-3
,共3页
何晓恩%何丽姗%罗健东%吴晓倩
何曉恩%何麗姍%囉健東%吳曉倩
하효은%하려산%라건동%오효천
机械牵张%自噬%LC3%Beclin-1%Akt
機械牽張%自噬%LC3%Beclin-1%Akt
궤계견장%자서%LC3%Beclin-1%Akt
mechanical stretch%autophagy%LC3%Beclin-1%Akt
目的：探讨机械牵张对血管平滑肌细胞自噬相关蛋白( LC3、Beclin-1)表达的影响及其机制。方法：机械牵张(10％牵张幅度，频率1Hz)处理血管平滑肌细胞进行不同时间(0-6 h)，Western blotting法检测LC3、Beclin-1，Akt、AMPK蛋白表达。结果：机械牵张处理血管平滑肌细胞自噬相关蛋白表达增加，Beclin-1蛋白30 min后表达最高( P<0.05)，LC3B II/I蛋白1 h后表达最高( P<0.05)。处理1 h后Akt磷酸化表达逐渐下降，AMPK磷酸化表达无明显变化。结论：机械牵张能增加自噬相关蛋白LC3、Beclin-1表达，可能与PI3K/Akt/mTOR路径有关。
目的：探討機械牽張對血管平滑肌細胞自噬相關蛋白( LC3、Beclin-1)錶達的影響及其機製。方法：機械牽張(10％牽張幅度，頻率1Hz)處理血管平滑肌細胞進行不同時間(0-6 h)，Western blotting法檢測LC3、Beclin-1，Akt、AMPK蛋白錶達。結果：機械牽張處理血管平滑肌細胞自噬相關蛋白錶達增加，Beclin-1蛋白30 min後錶達最高( P<0.05)，LC3B II/I蛋白1 h後錶達最高( P<0.05)。處理1 h後Akt燐痠化錶達逐漸下降，AMPK燐痠化錶達無明顯變化。結論：機械牽張能增加自噬相關蛋白LC3、Beclin-1錶達，可能與PI3K/Akt/mTOR路徑有關。
목적：탐토궤계견장대혈관평활기세포자서상관단백( LC3、Beclin-1)표체적영향급기궤제。방법：궤계견장(10％견장폭도，빈솔1Hz)처리혈관평활기세포진행불동시간(0-6 h)，Western blotting법검측LC3、Beclin-1，Akt、AMPK단백표체。결과：궤계견장처리혈관평활기세포자서상관단백표체증가，Beclin-1단백30 min후표체최고( P<0.05)，LC3B II/I단백1 h후표체최고( P<0.05)。처리1 h후Akt린산화표체축점하강，AMPK린산화표체무명현변화。결론：궤계견장능증가자서상관단백LC3、Beclin-1표체，가능여PI3K/Akt/mTOR로경유관。
Objective:To investigate the effects and mechanisms of mechanical stretch on autophagy-related proteins ( LC3,Beclin-1) expression in vascular smooth muscle cells. Methods: Vascular smooth muscle cells were stretched by mechanical stretch ( elongation=10%, frequency=1Hz) for 0 to 6 hours. The expression of LC3,Beclin-1,Akt and AMPK was detected by Western blotting. Results:The expression of autophagy-related proteins was increased after mechanical stretch in vascular smooth muscle cells. There was culmination of Beclin-1 at 30 minutes and LC3B II/I at 1 hour ( both P<0.05) . Mechanical stretch resulted in attenuated expression of phosphorylated Akt yet no marked variation in the expression of phosphorylated AMPK at hour 1. Conclusion:Mechanical stretch increases the expression of LC3 and Beclin-1 possibly related to the PI3K/Akt/mTOR pathway.
