{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,11]],"date-time":"2026-08-11T13:09:08Z","timestamp":1786453748069,"version":"build-2736575974"},"reference-count":47,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2019,6,12]],"date-time":"2019-06-12T00:00:00Z","timestamp":1560297600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2019,6,12]],"date-time":"2019-06-12T00:00:00Z","timestamp":1560297600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Cellular Biochemistry"],"published-print":{"date-parts":[[2019,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>The purpose of this study was to elucidate the expression of the long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) in rats with Alzheimer's disease (AD) and to explore its potential mechanisms.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      An AD rat model was induced by microinjection of A\u03b2\n                      <jats:sub>25\u201035<\/jats:sub>\n                      . On the first day after successful modeling, pcDNA3.1 plasmid and pcDNA3.1\u2010MEG3 plasmid were continuously infused into the third ventricle through a micro\u2010osmotic pump to interfere with the expression level of MEG3. The spatial learning ability and memory ability, the histopathological changes of hippocampus tissues, the ultrastructure of hippocampal neurons, astrocyte activation as well as the survival and apoptosis of hippocampal neurons in each group was observed. The expression of apoptosis, PI3\/Akt signaling pathway\u2010related proteins, glial fibrillary acidic protein, inflammatory factors, malondialdehyde, glutathione\u2010peroxidase, and superoxide dismutase levels were determined. The deposition of amyloid beta (A\u03b2) in the hippocampus of rats by was observed by A\u03b2 immunohistochemical staining.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Downregulated MEG3 was detected in the tissues of AD rats. In addition, upregulation of MEG3 contributed to an improvement of spatial learning ability and memory ability, inhibited the pathological injury and its apoptosis of hippocampal neurons, decreased A\u03b2 positive expression, inhibited oxidative stress injury and inflammatory injury as well as the activated astrocytes in AD rats via inactivation of the PI3\/Akt pathway.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our study highlights that upregulation of the lncRNA MEG3 improves cognitive impairment, alleviates neuronal damage, and inhibits activation of astrocytes in hippocampus tissues in AD through inhibiting the PI3K\/Akt signaling pathway.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/jcb.29108","type":"journal-article","created":{"date-parts":[[2019,6,13]],"date-time":"2019-06-13T00:52:22Z","timestamp":1560387142000},"page":"18053-18065","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":130,"title":["Upregulation of the lncRNA MEG3 improves cognitive impairment, alleviates neuronal damage, and inhibits activation of astrocytes in hippocampus tissues in Alzheimer's disease through inactivating the PI3K\/Akt signaling pathway"],"prefix":"10.1002","volume":"120","author":[{"given":"Jiping","family":"Yi","sequence":"first","affiliation":[{"name":"Department of Neurology, Translational Medicine Institute, The First People's Hospital of Chenzhou University of South China  Chenzhou P.R. 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