Shui Yu, Zhangming Zhou, Zhang Liang, Chenbin Ruan, Lei Bai, Ying Pi
{"title":"沉默lncRNA GABPB1-AS1可通过miR-641/NUCKS1轴减轻脑缺血再灌注损伤","authors":"Shui Yu, Zhangming Zhou, Zhang Liang, Chenbin Ruan, Lei Bai, Ying Pi","doi":"10.62347/EAGK7098","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>To investigate the possible mechanism of lncRNA GA binding protein transcription factor beta subunit 1 antisense RNA 1 (GABPB1-AS1) in cerebral ischemia/reperfusion (CI/R) injury.</p><p><strong>Methods: </strong>RT-qPCR was applied to determine GABPB1-AS1 expression in oxygen-glucose deprivation/reoxygenation (OGD/R) cells. The targeting relationships between GABPB1-AS1 and miR-641, as well as between miR-641 and nuclear casein and cyclin-dependent kinase substrate 1 (NUCKS1) were examined by dual luciferase reporter assay. The protein expression of caspase-3, Bax, Bcl-2 and NUCKS1 was examined by western blot. Cell apoptosis was measured by flow cytometry (FCM) and western blot. Cell viability was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.</p><p><strong>Results: </strong>GABPB1-AS1 was significantly elevated in SH-SY5Y cells under OGD/R. Downregulation of GABPB1-AS1 accelerated cell viability and suppressed cell apoptosis. GABPB1-AS1 silencing reduced ROS and MDA levels in OGD/R-treated cells. Furthermore, miR-641 inhibitor aggravated damage from OGD/R, but GABPB1-AS1 silencing notably attenuated this effect. NUCKS1 was proven to be a target gene of miR-641.</p><p><strong>Conclusion: </strong>GABPB1-AS1 silencing alleviated CI/R injury through the miR-641/NUCKS1 axis, indicating that GABPB1-AS1 might serve as a therapeutic target for CI/R injury.</p>","PeriodicalId":7731,"journal":{"name":"American journal of translational research","volume":null,"pages":null},"PeriodicalIF":1.7000,"publicationDate":"2024-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11301495/pdf/","citationCount":"0","resultStr":"{\"title\":\"Silencing lncRNA GABPB1-AS1 alleviates cerebral ischemia reperfusion injury through the miR-641/NUCKS1 axis.\",\"authors\":\"Shui Yu, Zhangming Zhou, Zhang Liang, Chenbin Ruan, Lei Bai, Ying Pi\",\"doi\":\"10.62347/EAGK7098\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>To investigate the possible mechanism of lncRNA GA binding protein transcription factor beta subunit 1 antisense RNA 1 (GABPB1-AS1) in cerebral ischemia/reperfusion (CI/R) injury.</p><p><strong>Methods: </strong>RT-qPCR was applied to determine GABPB1-AS1 expression in oxygen-glucose deprivation/reoxygenation (OGD/R) cells. The targeting relationships between GABPB1-AS1 and miR-641, as well as between miR-641 and nuclear casein and cyclin-dependent kinase substrate 1 (NUCKS1) were examined by dual luciferase reporter assay. The protein expression of caspase-3, Bax, Bcl-2 and NUCKS1 was examined by western blot. Cell apoptosis was measured by flow cytometry (FCM) and western blot. Cell viability was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.</p><p><strong>Results: </strong>GABPB1-AS1 was significantly elevated in SH-SY5Y cells under OGD/R. Downregulation of GABPB1-AS1 accelerated cell viability and suppressed cell apoptosis. GABPB1-AS1 silencing reduced ROS and MDA levels in OGD/R-treated cells. Furthermore, miR-641 inhibitor aggravated damage from OGD/R, but GABPB1-AS1 silencing notably attenuated this effect. NUCKS1 was proven to be a target gene of miR-641.</p><p><strong>Conclusion: </strong>GABPB1-AS1 silencing alleviated CI/R injury through the miR-641/NUCKS1 axis, indicating that GABPB1-AS1 might serve as a therapeutic target for CI/R injury.</p>\",\"PeriodicalId\":7731,\"journal\":{\"name\":\"American journal of translational research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.7000,\"publicationDate\":\"2024-07-15\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11301495/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"American journal of translational research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.62347/EAGK7098\",\"RegionNum\":4,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2024/1/1 0:00:00\",\"PubModel\":\"eCollection\",\"JCR\":\"Q3\",\"JCRName\":\"MEDICINE, RESEARCH & EXPERIMENTAL\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"American journal of translational research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.62347/EAGK7098","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
Silencing lncRNA GABPB1-AS1 alleviates cerebral ischemia reperfusion injury through the miR-641/NUCKS1 axis.
Objective: To investigate the possible mechanism of lncRNA GA binding protein transcription factor beta subunit 1 antisense RNA 1 (GABPB1-AS1) in cerebral ischemia/reperfusion (CI/R) injury.
Methods: RT-qPCR was applied to determine GABPB1-AS1 expression in oxygen-glucose deprivation/reoxygenation (OGD/R) cells. The targeting relationships between GABPB1-AS1 and miR-641, as well as between miR-641 and nuclear casein and cyclin-dependent kinase substrate 1 (NUCKS1) were examined by dual luciferase reporter assay. The protein expression of caspase-3, Bax, Bcl-2 and NUCKS1 was examined by western blot. Cell apoptosis was measured by flow cytometry (FCM) and western blot. Cell viability was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay.
Results: GABPB1-AS1 was significantly elevated in SH-SY5Y cells under OGD/R. Downregulation of GABPB1-AS1 accelerated cell viability and suppressed cell apoptosis. GABPB1-AS1 silencing reduced ROS and MDA levels in OGD/R-treated cells. Furthermore, miR-641 inhibitor aggravated damage from OGD/R, but GABPB1-AS1 silencing notably attenuated this effect. NUCKS1 was proven to be a target gene of miR-641.
Conclusion: GABPB1-AS1 silencing alleviated CI/R injury through the miR-641/NUCKS1 axis, indicating that GABPB1-AS1 might serve as a therapeutic target for CI/R injury.
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