TY - JOUR A2 - Manaenko，阿纳托尔AU - 兰蕊AU - 张咏AU - 吴涛AU - 马，云志AU - 王，宝齐AU - 郑海忠AU - 李，宝丽雅娜AU - 王，燕AU - 顾春青AU - 乌，吉涛PY年 - 2018年DA - 2018年6月19日TI - 小许明汤降低自噬激活和脑缺血再灌注改善线粒体功能损伤SP - 4147502 VL - 2018 AB - 我们研究了小许明水煎是否减少自噬激活，并保持在脑缺血再灌注损伤线粒体功能。Rats were randomly divided into 5 groups: sham, ischemia and reperfusion (IR), IR plus XXMD (60 g/kg/day) (XXMD60), IR plus cyclosporin A (10 mg/kg/day) (CsA), and IR plus vehicle (Vehicle). Focal cerebral ischemia and reperfusion models were induced by middle cerebral artery occlusion (MCAO). Cerebral infarct areas were measured by triphenyl tetrazolium chloride staining. Cerebral ischemic injury was evaluated by hematoxylin and eosin staining (HE) and Nissl staining. Ultrastructural features of mitochondria and mitophagy in the penumbra of the ischemic cortex were observed by transmission electron microscopy. Mitophagy was detected by immunofluorescence labeled with LC3B and VDAC1. Autophagy lysosome formation was observed by immunofluorescence labeled with LC3B and Lamp1. The expression of LC3B, Beclin1, and Lamp1 was analyzed by Western blot. The rats subjected to MCAO showed worsened neurological score and cell ischemic damage. These were all significantly reversed by XXMD or CsA. Moreover, XXMD/CsA notably downregulated mitophagy and reduced the increase in LC3, Beclin1, and Lamp1 expression induced by cerebral ischemia and reperfusion. The findings demonstrated that XXMD exerted neuroprotective effect via downregulating LC3, Beclin1, Lamp1, and mitochondrial p62 expression level, thus leading to the inhibition of mitophagy. SN - 0953-4180 UR - https://doi.org/10.1155/2018/4147502 DO - 10.1155/2018/4147502 JF - Behavioural Neurology PB - Hindawi KW - ER -