{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,14]],"date-time":"2026-10-14T06:16:47Z","timestamp":1791958607719,"version":"4.3.4"},"reference-count":50,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2020,2,10]],"date-time":"2020-02-10T00:00:00Z","timestamp":1581292800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2020,6]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>MicroRNAs (miRNAs) have emerged as critical regulators of neuronal survival during cerebral ischaemia\/reperfusion injury. Accumulating evidence has shown that miR\u2010199a\u20105p plays a crucial role in regulating apoptosis and survival in various cell types. However, whether miR\u2010199a is involved in regulating neuronal survival during cerebral ischaemia\/reperfusion injury remains unknown. In this study, we aimed to explore the biological role of miR\u2010199a\u20105p in regulating neuronal injury induced by oxygen\u2010glucose deprivation\/reoxygenation (OGD\/R), an in vitro cellular model of cerebral ischaemia and reperfusion injury. We found that miR\u2010199a\u20105p expression was significantly altered in neurons in response to OGD\/R treatment. Overexpression of miR\u2010199a\u20105p facilitated OGD\/R\u2010induced apoptosis and reactive oxygen species (ROS) production, whereas miR\u2010199a\u20105p inhibition alleviated OGD\/R\u2010induced apoptosis and ROS production. Notably, our results identified Brahma\u2010related gene 1 (Brg1) as a target gene of miR\u2010199a\u20105p. Moreover, inhibition of miR\u2010199a\u20105p promoted the activation of nuclear factor\u2010erythroid\u20102\u2010related factor\u20102 (Nrf2)\/heme oxygenase\u20101 (HO\u20101) signalling via targeting Brg1. However, silencing of Brg1 markedly reversed the miR\u2010199a\u20105p inhibition\u2010mediated neuroprotective effect. Taken together, our results suggest that downregulation of miR\u2010199a\u20105p protects neurons from OGD\/R\u2010induced neuronal injury through upregulating Brg1 to activate Nrf2\/HO\u20101 signalling. The miR\u2010199a\u20105p\/Brg1\/Nrf2\/HO\u20101 regulation axis may play an important role in regulating neuronal survival during cerebral ischaemic\/reperfusion injury in vivo.<\/jats:p>","DOI":"10.1111\/1440-1681.13265","type":"journal-article","created":{"date-parts":[[2020,1,28]],"date-time":"2020-01-28T17:35:55Z","timestamp":1580232955000},"page":"1020-1029","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Inhibition of microRNA\u2010199a\u20105p ameliorates oxygen\u2010glucose deprivation\/reoxygenation\u2010induced apoptosis and oxidative stress in HT22 neurons by targeting Brg1 to activate Nrf2\/HO\u20101 signalling"],"prefix":"10.1111","volume":"47","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2695-7228","authenticated-orcid":false,"given":"Feng","family":"Li","sequence":"first","affiliation":[{"name":"Anesthesiology Department The First Affiliated Hospital of Xi'an Jiaotong University Xi'an 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