TY -的A2 Pospisil帕维尔AU -杨,郑AU -吴,青青AU -肖,杨AU -段,明夏盟——刘、陈盟——元,元盟——孟,欣欣盟——廖,海汉盟——唐,启朱PY - 2018 DA - 2018/06/25 TI - Aucubin防止心肌Infarction-Induced心脏重构通过nNOS / NO-Regulated氧化应激SP - 4327901六世- 2018 AB - Aucubin是否能保护心肌梗死(MI)诱导的心脏重建还不清楚。在这项研究中,在老鼠模型中,心脏重构是引起冠状动脉左前降枝结扎手术。小鼠腹腔注射aucubin mi(10毫克/公斤)3天。mi后两周,老鼠aucubin治疗组显示降低死亡率,减少梗塞面积,改善心脏功能。Aucubin也减少了心脏重塑mi。一致,aucubin体外心肌细胞对缺氧损伤的保护。从力学上看,我们发现aucubin抑制ASK1 /物信号。这些影响被物取消激活。此外,我们发现氧化应激是减毒在体内aucubin-treated小鼠心脏和vitro-treated心肌细胞,导致减少硫氧还蛋白(硫氧还蛋白)消费,导致ASK1形成硫氧还蛋白的复杂活动。在体内和体外Aucubin nNOS-derived没有增加生产。 The protective effects of aucubin were reversed by the NOS inhibitors L-NAME and L-VINO in vitro. Furthermore, nNOS knockout mice also reversed the protective effects of aucubin on cardiac remodeling. Taken together, aucubin protects against cardiac remodeling post-MI through activation of the nNOS/NO pathway, which subsequently attenuates the ROS production, increases Trx preservation, and leads to inhibition of the ASK1/JNK pathway. SN - 1942-0900 UR - https://doi.org/10.1155/2018/4327901 DO - 10.1155/2018/4327901 JF - Oxidative Medicine and Cellular Longevity PB - Hindawi KW - ER -