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作 者:An-Qi Zhang Lu Wang Yi-Xiu Wang Shan-Shan Hong Yu-Shan Zhong Ru-Yi Yu Xin-Lu Wu Bing-Bing Zhou Qi-Min Yu Hai-Feng Fu Shuang-Dong Chen Yun-Chang Mo Qin-Xue Dai Jun-Lu Wang
机构地区:[1]Department of Anesthesiology,The First Affiliated Hospital of Wenzhou Medical University,Wenzhou,Zhejiang Province,China [2]Department of Anesthesiology,Wenzhou Central Hospital,Wenzhou,Zhejiang Province,China
出 处:《Neural Regeneration Research》2022年第11期2504-2511,共8页中国神经再生研究(英文版)
基 金:funded by the National Natural Science Foundation of China,No.81803937(to YCM and QXD);Science and Technology Innovation Activity Plan for College Students of Zhejiang Province(Xinmiao Talent Plan),No.2020R413079(to AQZ);Wenzhou Science and Technology Plan Project,No.Y20210122(to QXD)。
摘 要:Previous studies have suggested that miR-324-3p is related to the pathophysiology of cerebral ischemia,but the mechanism underlying this relationship is unclea r.In this study,we found that miR-324-3p expression was decreased in patients with acute ischemic stroke and in in vitro and in vivo models of ischemic stro ke.miR-324-3p agomir potentiated ischemic brain damage in rats subjected to middle cerebral artery occlusion,as indicated by increased infarct volumes and cell apoptosis rates and greater neurological deficits.In a PC12 cell oxygen-glucose deprivation/reoxygenation model,a miR-324-3 p mimic decreased cell viability and expression of the anti-apoptotic protein BCL2 and increased expression of the pro-apoptotic protein BAX and rates of cell apoptosis,whereas treatment with a miR-324-3p inhibitor had the opposite effects.Silencing miR-324-3p increased adenosine A1 receptor(A1R)expression thro ugh regulation of GATA binding protein 2(GATA2).These findings suggest that silencing miR-324-3p reduces ischemic brain damage via the GATA2/A1R axis.
关 键 词:acute ischemic stroke adenosine A1 receptor apoptosis cerebral ischemia-reperfusion injury cortical neurons GATA2 middle cerebral artery occlusion miR-324-3p oxygen-glucose deprivation/reoxygenation PC12 cells
分 类 号:R743.3[医药卫生—神经病学与精神病学]
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