CAJ | 학술논문

目的：探讨芹菜素( apigenin, Api)在心肌细胞缺氧/复氧损伤中的作用,并阐明Api对心肌损伤的保护作用是否主要由Bcl-2介导。方法培养H9c2心肌样细胞；随机分为正常对照( Cont )组、缺氧/复氧( Anoxia/Reoxygenation, A/R)组、Api预处理组、Api+ABT-737组。 MTT法检测细胞存活率；Western blot法检测Bcl-2表达；比色法检测培养液LDH活性、细胞SOD及GSH-Px活性、MDA含量；流式细胞仪检测心肌细胞 ROS 含量、线粒体膜电位及细胞凋亡。结果 Api预处理25 h后,心肌细胞Bcl-2表达呈剂量依赖性上调( P <0．01)；细胞存活率升高,培养液 LDH 活性降低,细胞SOD、GSH-Px 活性升高, MDA 含量与 ROS 生成减少,线粒体膜电位更为稳定,细胞凋亡减少( P<0．01)；Bcl-2抑制剂ABT-737则可取消Api的上述心肌保护作用。结论Api抗心肌A/R损伤作用涉及Bcl-2信号通路,至少部分依赖于其对Bcl-2表达水平的上调。
목적：탐토근채소( apigenin, Api)재심기세포결양/복양손상중적작용,병천명Api대심기손상적보호작용시부주요유Bcl-2개도。방법배양H9c2심기양세포；수궤분위정상대조( Cont )조、결양/복양( Anoxia/Reoxygenation, A/R)조、Api예처리조、Api+ABT-737조。 MTT법검측세포존활솔；Western blot법검측Bcl-2표체；비색법검측배양액LDH활성、세포SOD급GSH-Px활성、MDA함량；류식세포의검측심기세포 ROS 함량、선립체막전위급세포조망。결과 Api예처리25 h후,심기세포Bcl-2표체정제량의뢰성상조( P <0．01)；세포존활솔승고,배양액 LDH 활성강저,세포SOD、GSH-Px 활성승고, MDA 함량여 ROS 생성감소,선립체막전위경위은정,세포조망감소( P<0．01)；Bcl-2억제제ABT-737칙가취소Api적상술심기보호작용。결론Api항심기A/R손상작용섭급Bcl-2신호통로,지소부분의뢰우기대Bcl-2표체수평적상조。
Aim To investigate the relationship be-tween the cardioprotection of apigenin ( Api ) from an-oxia/reoxygenation ( A/R) injury and Bcl-2 pathway. Methods H9 c2 cardiomyocytes were cultured and di-vided into normal control group, A/R group, Api pre-treatment group ( Api ) , Api + Bcl-2 inhibitor group ( Api + ABT-737 ) . Expression of Bcl-2 was deter-mined by Western blot,and cell viability was measured by MTT method. LDH, SOD, GSH-Px, MDA activity were determined by chromometry. ROS generation, mi-tochondrial membrane potential and apoptosis were de-termined by flow cytometry. Results 25h after apige-nin precondition,the expression of Bcl-2 was upregulat-ed in cardiomyocytes ( P <0. 01 ) . In the group pre-treated with 40 μmol · L-1 apigenin before A/R, the activity of LDH in culture medium decreased; the ac-tivity of intracellular SOD, GSH-Px increased; the content of MDA and ROS generation decreased; cell viability increased; mitochondrial membrane potential could be more stable and cell apoptosis decreased ( P<0. 01 ) . However, all these protective effects were attenuated significantly in the group pretreated with apigenin and Bcl-2 inhibitor ABT-737 . Conclusion The effect of apigenin against A/R injury in cardiomyo-cytes involves Bcl-2 pathway, and at least partly de-pends on its effect on upregulating the expression of Bcl-2 .