CAJ | 학술논문

目的：探讨丹皮酚对鱼藤酮诱导SH- SY5Y细胞凋亡的保护作用及其机制。方法采用不同浓度丹皮酚预处理SH- SY5Y细胞，加入鱼藤酮诱导建立帕金森病（PD）神经元损伤模型，以CCK-8检测细胞增殖活性，流式细胞术检测细胞凋亡，组织活性氧荧光定量法（DCFH- DA法）检测细胞内活性氧（ROS）生成，并以JC-1染色检测线粒体膜电位（MMP），同时检测凋亡相关蛋白半胱氨酸天冬氨酸特异性蛋白酶-3（caspase-3）活性。结果1μmol/L鱼藤酮处理24 h后SH- SY5Y细胞增殖活性显著降低，凋亡细胞数增多，ROS生成增加，MMP降低，caspase-3活性升高（均P＜0.01），说明PD神经元损伤模型建立成功。与鱼藤酮处理组比较，丹皮酚(5、25μmol/L)预处理后SH- SY5Y细胞增殖活性提高，凋亡细胞数减少，ROS生成受到抑制，MMP改善，而caspase-3活性降低（P＜0.05或0.01）。结论丹皮酚(5、25μmol/L)对鱼藤酮诱导的SH- SY5Y细胞凋亡具有抑制作用，其机制可能与丹皮酚的抗氧化作用等有关。
목적：탐토단피분대어등동유도SH- SY5Y세포조망적보호작용급기궤제。방법채용불동농도단피분예처리SH- SY5Y세포，가입어등동유도건립파금삼병（PD）신경원손상모형，이CCK-8검측세포증식활성，류식세포술검측세포조망，조직활성양형광정량법（DCFH- DA법）검측세포내활성양（ROS）생성，병이JC-1염색검측선립체막전위（MMP），동시검측조망상관단백반광안산천동안산특이성단백매-3（caspase-3）활성。결과1μmol/L어등동처리24 h후SH- SY5Y세포증식활성현저강저，조망세포수증다，ROS생성증가，MMP강저，caspase-3활성승고（균P＜0.01），설명PD신경원손상모형건립성공。여어등동처리조비교，단피분(5、25μmol/L)예처리후SH- SY5Y세포증식활성제고，조망세포수감소，ROS생성수도억제，MMP개선，이caspase-3활성강저（P＜0.05혹0.01）。결론단피분(5、25μmol/L)대어등동유도적SH- SY5Y세포조망구유억제작용，기궤제가능여단피분적항양화작용등유관。
Objective To investigate the effects of paeonol on rotenone- induced apoptosis in SH- SY5Y cells. Methods SH- SY5Y cells were pretreated with paeonol and then rotenone was added in the culture medium. cellviability was detected by CCK- 8 assay. The apoptosis rate was assessed by flow cytometry. Cellular ROS production were detected by DCFH- DA. The mitochondial membrane potential (MMP) was determined by JC- 1 staining and the caspase- 3 activity was measured by cas-pase- 3 kit. Results 1μmol/L rotenone significantly decreased cellviability, enhanced the apoptotic rate and overproduced ROS, reduced MMP and increased caspase- 3 activity. Compared to rotenone treated group, 5,25μmol/L paeonol significantly ameliorated celldamage, inhibited apoptotic rate and ROS overproduction, al eviated the decrease of MMP and reduced the caspase- 3 activity. Conclusion Paeonol can prevent SH- SY5Y cells from apoptosis induced by rotenone, which may be as-sociated with its anti- oxidant ability.