CAJ | 학술논문

目的：探讨光果甘草定（Glabridin，GD）对氧化型低密度脂蛋白（ox-LDL）损伤性的细胞中自噬（ autophagy ）的影响。方法：采用体外培养人主动脉内皮细胞（ HAVEC ），经不同浓度GD预处理或不预处理，再行ox-LDL干预作对比。 MTT法检测细胞活性、透射电镜观察细胞中自噬小体，免疫印迹检自噬相关蛋白Beclin1和LC3在不同组别中的表达。结果：随ox-LDL浓度的增加，细胞活性，细胞中自噬小体和Beclin1和LC3的表达比空白对照组明显增加（P＜0．05）。经GD预处理的HAVEC，细胞活性，自噬小体和Beclin1和LC3的表达比未经GD预处理细胞组明显降低（ P＜0．05）。结论：ox-LDL能浓度依赖性地诱导HAVEC自噬性死亡，GD通过部分抑制自噬相关因子，保护血管内皮细胞。
목적：탐토광과감초정（Glabridin，GD）대양화형저밀도지단백（ox-LDL）손상성적세포중자서（ autophagy ）적영향。방법：채용체외배양인주동맥내피세포（ HAVEC ），경불동농도GD예처리혹불예처리，재행ox-LDL간예작대비。 MTT법검측세포활성、투사전경관찰세포중자서소체，면역인적검자서상관단백Beclin1화LC3재불동조별중적표체。결과：수ox-LDL농도적증가，세포활성，세포중자서소체화Beclin1화LC3적표체비공백대조조명현증가（P＜0．05）。경GD예처리적HAVEC，세포활성，자서소체화Beclin1화LC3적표체비미경GD예처리세포조명현강저（ P＜0．05）。결론：ox-LDL능농도의뢰성지유도HAVEC자서성사망，GD통과부분억제자서상관인자，보호혈관내피세포。
Objective:To investigate the anti -atherosclerosis mechanism of Glabridin ( GD) whether via the pathway of autophagy.Methods:The cultured human aorta vascular endothelial cells (HAVECs)were pretreated with or without dif-ferent concentrations of GD , then treated with different concentrations of ox -LDL to induce cell injury or autophagy . The detection of cell viability by MTT assay , autophagic bodies by transmission electron microscopy , and autophagy -re-lated protein Beclin1 and LC3 by Western blotting were conducted in different groups .Results:Dose-correlated signifi-cant decrease in cell viability was observed in ox -LDL treated HAVECs than that in blank control group , while the au-tophagic body and the expressions of Beclin 1 and LC3 significantly increased compared with the control group ( P<0.05 ) .By contrast , the HAVEC pretreated by GD exhibited considerable higher in cell viability than the ox -LDL counterparts, while the expressions of autophagic bodies and Beclin 1 and LC3 were significantly lower (P<0.05). Conclusion:The concentration-dependent ox-LDL can induce autophagic death of HAVEC ,and the protective actions of vascular cells or anti -AS effect of GD may be partially via the inhibition of autophagy pathway .