TY -的A2 Malendowicz Ludwik k . AU - Wang Jing盟——咚,Zhichun AU -卢Liyin AU -杨,Lijuan盟——秋,精英PY - 2021 DA - 2021/05/12 TI - mir - 122在STZ-Induced胰腺参与氧化应激和细胞凋亡β细胞通过调节PI3K / AKT信号通路SP - 5525112六世- 2021 AB -目前,很少有报道关于mir - 122和糖尿病之间的关系。此外,mir - 122对链脲霉素(STZ)——INS-1细胞诱导氧化损伤仍不清楚。本研究旨在调查涉及mir - 122的作用和调节机制在糖尿病。采用STZ诱导INS-1细胞损伤。反向transcription-quantitative PCR用于调查mir - 122的表达。TUNEL细胞凋亡检测设备用于检测细胞凋亡。使用dichlorofluorescein-diacetate细胞内ROS水平测定。胰岛素分泌的活动,超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(氧化酶)使用ELISA试剂盒测定。西方墨点法是用来测量伯灵顿的表达水平,bcl - 2, PI3K, p-PI3K, caspase-3 caspase-9, cleaved-caspase-3 cleaved-caspase-9, AKT, p-AKT。然后,LY294002 (LY, PI3K抑制剂)是用于治疗INS-1细胞氧化应激和细胞凋亡测定。 The results showed that STZ-induced inhibitory effects on insulin secretion were mitigated by miR-122 inhibitor, and the activities of SOD, CAT, and GSH-px were also increased. Furthermore, miR-122 inhibitor inhibited apoptosis and oxidative stress in STZ-induced INS-1 cells. Finally, the addition of LY increased insulin levels; reduced the activities of SOD, CAT, and GSH-px; and promoted apoptosis in STZ-induced INS-1 cells. In conclusion, interference with miR-122 can inhibit oxidative stress and apoptosis in STZ-induced INS-1 cells, involving a mechanism of action related to the PI3K/AKT pathway. SN - 1687-8337 UR - https://doi.org/10.1155/2021/5525112 DO - 10.1155/2021/5525112 JF - International Journal of Endocrinology PB - Hindawi KW - ER -