CAJ | 학술논문

目的：探讨表没食子儿茶素没食子酸酯(EGCG)对胰岛细胞的保护作用及机制。方法实验分为正常对照组,IL-1β组,IL-1β+EGCG1组(低浓度),IL-1β+ EGCG2组(高浓度)。CCK8检测细胞活性,酶联免疫吸附实验(ELISA)方法检测MIN6细胞基础胰岛素和葡萄糖刺激的胰岛素分泌量,Hochest 染色及流式细胞术检测细胞凋亡,JC-1流式细胞术检测线粒体膜电位,比色法测定细胞腺嘌呤核苷三磷酸(ATP)含量,化学荧光法检测细胞活性氧簇(ROS)活性。结果与正常对照组相比,IL-1β组细胞活性降低,基础和葡糖糖刺激胰岛素分泌量显著减少,细胞凋亡明显增加,同时测得细胞线粒体膜电位降低,ATP 含量减少,提示细胞线粒体功能损伤,并且 ROS 活性增加。给予低浓度和高浓度 EGCG 作用后,与 IL-1β组相比,细胞活性明显提高,基础和葡糖糖刺激胰岛素分泌量增加,细胞凋亡率显著减少,线粒体膜电位增加,ATP 含量增加,同时 ROS 活性降低。且 IL-1β+EGCG2组作用更强。结论EGCC 可减轻 IL-1β诱导的 MIN6细胞细胞凋亡率,其机制可能与提高细胞 ATP 的含量,线粒体膜电位及降低 ROS 活性有关。
목적：탐토표몰식자인다소몰식자산지(EGCG)대이도세포적보호작용급궤제。방법실험분위정상대조조,IL-1β조,IL-1β+EGCG1조(저농도),IL-1β+ EGCG2조(고농도)。CCK8검측세포활성,매련면역흡부실험(ELISA)방법검측MIN6세포기출이도소화포도당자격적이도소분비량,Hochest 염색급류식세포술검측세포조망,JC-1류식세포술검측선립체막전위,비색법측정세포선표령핵감삼린산(ATP)함량,화학형광법검측세포활성양족(ROS)활성。결과여정상대조조상비,IL-1β조세포활성강저,기출화포당당자격이도소분비량현저감소,세포조망명현증가,동시측득세포선립체막전위강저,ATP 함량감소,제시세포선립체공능손상,병차 ROS 활성증가。급여저농도화고농도 EGCG 작용후,여 IL-1β조상비,세포활성명현제고,기출화포당당자격이도소분비량증가,세포조망솔현저감소,선립체막전위증가,ATP 함량증가,동시 ROS 활성강저。차 IL-1β+EGCG2조작용경강。결론EGCC 가감경 IL-1β유도적 MIN6세포세포조망솔,기궤제가능여제고세포 ATP 적함량,선립체막전위급강저 ROS 활성유관。
Objective To investigate the effects of Epigallocatechin gallate(EGCG)on IL-1βinduced MIN6 cells apoptosis. M.Methods The experiment group was divided into control group,IL-1β group,IL-1β+ EGCG low concentration group and IL-1β+EGCG high concentration group.Cell activity was detected by CCK8.Insulin secretion was detected by ELISA.cell apoptosis was detected by flow cytometry.The mitochondrial membrane potential was detected by flow cytometry.ATP content and cell ac-tivity of ROS were detected by colorimetry and chemiluminescence method.Results Compared with normal group,IL-1β group showed much lower cell activity,insulin secretion,cell mitochondrial membrane potential and ATP content,and at the same time IL-1βgroup had significantly higher cell apoptosis and ROS activities.After given EGCG,both low concentration group and high con-centration group had higher cell activity,insulin secretion,cell mitochondrial membrane potential and ATP content,at the same time lower cell apoptosis and ROS activities was showed.And the IL-1β+EGCG high concentration group worked more powerful.Con-clusion EGCG has protective effects on IL-1βinduced MIN6 cells apoptosis.Its mechanism may be related to increasing the content of the ATP and mitochondrial membrane potential and protecting mitochondrial function as well reducing the activity of ROS.